JSM Tropical Medicine and Research

Galectin-3 Controls Inflammatory Responses during Schistosomiasis

Review Article | Open Access

  • 1. Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Brazil
+ Show More - Show Less
Corresponding Authors
Felipe L. Oliveira, Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Av. Carlos Chagas Filho, 343. Centro de Ciências da Saúde, Bloco F2 – sala 1, Phone: 55 21 39386483

Schistosomiasis affects 240 million people around the world. Schistosoma mansoni is the major infecting form and evokes a severe immune response after egg-deposition in the mesenteric venous system. In the liver, eggs induce a powerful fibrogranulomatous reaction by macrophage-dependent manner. These cells drive a robust TH1 immune response that progresses to acute TH2 response. Subsequently, chronic phase is hallmarked by liver fibrosis, hepato/splenomegaly and humoral immune response. S.mansoni synthesizes glycoconjugates which interact with galectin-3, a β-galactoside-binding protein that regulates cell-cell and cell-matrix interactions and this binding elicits inflammation and humoral response against the parasite. Using galectin-3-deficient mice (gal-3-/- mice), we have investigate the involvement of galectin-3 on the pathogenesis of schistosomiasis. Here, we discussed the possibility to use galectin-3 to interfere with distinct phases of schistosomiasis and proposed some targets: macrophage and B lymphocyte differentiation, IL-5 and TGF-β signaling pathways, IgM-to-IgA class switching and mast cell degranulation. We proposed that galectin-3 is a key element to drive immune responses against S.mansoni and consequently suggested this protein as potential pharmacological target.


Oliveira FL, El-Cheikh MC (2017) Galectin-3 Controls Inflammatory Responses during Schistosomiasis. JSM Trop Med Res 2(1): 1014.


•    Schistosomiasis
•    Galectin-3
•    Immune response
•    Lymphocytes
•    Macrophages


IL: Interleukin; TNF-α: Tumor Necrosis Factor – alpha; WT: Wild type; Gal-3-/- galectin-3 deficient mice; MLNs: Mesenteric lymph nodes


Schistosomiasis is a neglected-tropical disease affecting about 240 million people around the world. In Latin America, Schistosoma mansoni is the major infecting form when the aquaticlarval cercariae contact body superficies of individuals swimming in lagoons and dams [1]. After skin penetration, cercariae induce immune responses that drive schistosome maturation. The adult worms live in the mesenteric venous system in constant sexual reproduction and egg deposition. Generally, the eggs are expelled to intestinal lumen or trapped in the mesenteric vessels and hepatic portal zone [2].

The pathogenesis of the schistosomiasis is established by macrophage responses against S.mansoni-eggs accumulated in the liver resulting in portal inflammation and hypertension that cause liver fibrosis and failure in patients and experimental models, including mice [3]. Regarding to murine models, migrating immature worms (schistosomules) evoke a TH1 immune response 3 weeks after the infection that persist for approximately 20 days [4]. On day 45-50 post-infection, high levels of IL-4 and IL-5 drive the acute phase of schistosomiasis hallmarked by typical TH2 responses. On day 85-90 postinfection, the chronic phase is characterized by down-regulation of both cytokines and liver inflammation shifting from exudative response to fibrotic pattern [5]. Independently of the stage of the disease, lymphoid and myeloid cells are recruited to the liver or lymphoid organs in response to local and circulating antigens, respectively.


TH1 response is characterized by mobilization of bone marrow monocytes to mesenteric venous system reacting against schistosomules. Liver-resident macrophages (Kupffer cells) respond immediately to egg-deposition secreting proinflammatory cytokines IL-1 and TNF-α [6]. These cells modulate the formation of exsudative granulomas, hepatocyte functions and hepatic stellate cell activation [7]. In accordance, serum levels of TNF-α is significantly increased in humans with similar stage of the disease [8]. Pro-inflammatory Ly6ClowCD11b+ CCR2+ CX3CR1− and pro-fibrotic Ly6ChighCD11b+ CCR2− CX3CR1+ monocytes are involved with initial response in definitive hosts [9]. 

TH2 response is established by the presence of egg-antigens with local and systemic effects in the course of the acute phase. Although S.mansoni-eggs are continuously delivered in the mesenteric system and drained to the liver, the hepatic parenchyma remains functional because, at least in part, the concentric fibrogranulomatous reaction isolates the eggs and antigens [2]. However, soluble egg-antigens give the bloodstream and amplify the polyclonal B cell activation in secondary lymphoid tissues [5]. After day 40 post-infection, it is possible to observe germinal centers and enhancement of antibody production [10,11].


S.mansoni synthesizes GalNAc_1-4(Fuc_1-3)GlcNAc (Lac-DiNAc) structures (N-acetylgalactosamine _1-4 N-acetylglucosamine), glycoconjugates which interact with galectin-3 (Gal-3) produced by host-immune cells eliciting a robust immune response towards the parasite [12,13]. Gal-3 is a β-galactoside-binding protein that plays crucial roles in cellcell and cell-matrix interactions during inflammation, tumor progression and homeostasis. It is localized in extra or intracellular compartments suggesting complex multifunctionality, such as pro-inflammatory functions and cellular proliferation, respectively [14].

In the course of murine schistosomiasis, Gal-3 staining is positive within the granulomas, in Kupffer cells, and myelopoietic niches. Using gal-3-/- infected-mice, we observed that acute liver granulomas showed a productive-exudative pattern in contrast to necrotic-exsudative pattern observed in wild type (WT) mice. Moreover, in the absence of Gal-3, the pattern of collagen organization was disturbed with non-concentric fibers dispersed throughout the parenchyma and numerous myeloid cell niches abnormally distributed around the schistosomal eggs [15]. During the last decade, we demonstrated that Gal-3 is involved with pathogens of schistosomiasis regulating leukocyte mobilization from the bone marrow, macrophage functions and B lymphocyte differentiation in the spleen and mesenteric lymph nodes (MLNs), and inflammatory reaction in the peritoneal cavity in mice infected with S.mansoni [15-18].

Macrophages were significantly reduced whereas monocytes were significantly increased in the liver of gal-3-/- infected mice. Moreover, these monocytes poorly differentiated into macrophages in vitro. Furthermore, the number of B220+/ lowCD138+ plasma cells was substantially increased in the bone marrow [15].

Lymphocytes are frequently activated by adult worm- and egg-antigens drained to MLNs and spleen inducing a significant polyclonal B cell reaction [6]. In both organs of WT chronicallyinfected-mice, Gal-3 was detected in large non-lymphoid follicular cells and small/rounded extrafollicular cells [16,17]. MLNs of gal-3-/- infected mice presented higher number of clusters of B220+ B lymphocytes in the cortex, paracortex and medulla in comparison with WT mice. Moreover, CD138+ plasma cells were abnormally localized within lymphoid follicles and significantly increased in extrafollicular sites [16]. In the spleen, the absence of Gal-3 during schistosomiasis was correlated with intense white pulp reaction, and disorganized B lymphocyte and CD138+ plasma cell niches [17]. These histological data corroborated with serological aspects, since the high number of plasma cells in gal-3-/- infected-mice was associated with increased serum levels of IgG, IgE and IgA [15,18].

The peritoneal cavity has been considered a reservoir of circulating leukocytes (monocytes, T and B lymphocytes and granulocytes) and resident cells (macrophages, mast cells and B lymphocytes) frequently detected attached in the omentum and mesentery [19,20]. These cells react promptly against the presence of S.mansoni antigens resulting in macrophage hyperactivity and B cell activation leading to IgM-to-IgE class switching [11,21,22]. The mesentery and omentum of gal-3-/- chronically-infected mice were enriched by clusters of CD138+ plasma cells and Blimp-1+ immunoglobulin-secreting plasma cells, directly correlated with high levels of serum IgA as well as with peritoneal B1 lymphocyte differentiation into IgA-secreting plasma cells by IL-5 and TGF-β dependent manner [18].


In order to investigate possible molecular mechanisms involving Gal-3 and the pathogenesis of schistosomiasis, IL-5 and TGF-β pathways could be interesting targets. S.mansoni expresses SmRK1a (TGF-β receptor) suggesting a possible immunomodulation by hosts [23]. Moreover, TGF-β-mediated myofibroblast activation and matrix production were significantly inhibited in gal-3-/- mice induced to chronic liver fibrosis [24]. IL-5 gene expression is down-regulated by Gal-3 in distinct cell types [25]. In addition, both cytokines are essentials for IgM-toIgA-class switching [26].

Cellular mechanisms are also interesting strategies to understand and control the evolution of schistosomiasis and other parasitic diseases. Regarding to Gal-3, our data indicated monocyte-macrophage and B lymphocyte-plasma cell differentiation as possible cellular targets. However, growing evidence pointed to mast cells as potential cell target involving Gal-3 and the pathogenesis of schistosomiasis. Considering that mast cells enhance B cell expansion and differentiation into IgA-producing plasma cells [27], we investigated a possible correlation between these cells, Gal-3 and IgA levels found in gal-3-/- S.mansoni-infected mice. In these mice, peritoneal mast cells were frequently degranulated indicating an enhanced stage of activation. In fact, the in vitro and in vivo treatment with IL-5+TGF-β1 induced an increase in mast cell number and degranulation status, both associated with elevated number of peritoneal IgA+ B cells in the absence of Gal-3 [18].

The synergistic IL-5/TGF-β1 effects can be studied in the near future, in order to test therapeutic strategies based on cytokines against S. mansoni. In contrast, each cytokine alone does not offer an effective therapy. Helminth-infected mice over expressing IL-5 presented intense eosinophilia, but inflammatory and antibody responses were similar to wild type mice [28]. Eosinophil-ablated mice and control littermates were equivalent on egg deposition, liver fibrosis and serum-hepatic enzymes [29]. Moreover, IL-5 deficient mice presented smaller granulomas completely devoid of eosinophils and approximately 40% of reduction in hepatic fibrosis [30].

TGF-β1 is considered a fibrogenic mediator in schistosomiasis synthesized by granuloma cells [31]. However, studies with TGF-β1−/− mice indicated the existence of TGF-β1 independent liver fibrosis induced by infection [32]. The possible use of TGF- β1 as therapeutic strategy was firstly discussed after the identification of this cytokine controlling embryogenic events of S. mansoni [33]. On the other hand, serum and hepatic TGF- β1 levels are significantly reduced after treatment with anti-parasite drugs [34,35]. In the liver granulomas, TGF- β1 activates hepatic stellate cells (HSCs) which secrete inflammatory metabolites, such as cystenil leukotrienes and prostaglandin D2 [36,37]. Recently, it was demonstrated that hepatic granuloma derived myofibroblasts of S. mansoni-infected mice were able to secrete IL-5 and eotaxin after TGF-β1 and IL-13 stimulation [38].

In this context, Gal-3 would be analyzed as mediator of pathways that control hepatic stallate cells/myofibroblast activation, and possible interference with IL-5 and TGF-β1 secretion. Gal-3 is up-regulated in HSCs during their differentiation into myofibroblasts [24] and recombinant Gal3 induced hepatic stellate cell proliferation [39]. Furthermore, Gal-3 favors phagocytosis by HSCs and liver fibrosis in vivo [40]. Recently, we suggested that myofibroblasts are potential cellular targets to control liver fibrosis in the course of schistosomiasis by linking multiple/complex signaling mechanisms: Gal-3, epigenetic factors (such as histone deacetylases) and sonic hedgehog [41].


Schistosomiasis is a complex helminthic disease that induces a robust systemic immune response and fibrogranulomatous reaction in the liver. Currently, Gal-3 has been described as potent modulator of cell-cell and cell-extracellular matrix interactions, critical events to establishment of pathogenesis of schistosomiasis. Data obtained during the last decade pointed to macrophages, plasma cells and mast cells as possible cellular targets of Gal-3. The differentiation and functions of these cell types were severely disturbed during schistosomiasis evolution in the absence of Gal-3. Moreover, Gal-3 is involved with IL-5 and TGF-β expression, indicating that both cytokines can be added to the list of possible molecular targets of Gal-3 during schistosomiasis. Together, data discussed here suggested that Gal-3 negatively regulates B cell differentiation into plasma cells, induces monocyte differentiation into macrophages and controls mast cell activation by IL-5/TGF-β dependent manner during schistosomiasis. We concluded that Gal-3 is a key element to drive cell fate decision during S.mansoni-infection, consequently, a potential pharmacological target to future studies and treatment of schistosomiasis.


The authors contributed equally to this work.


1. Andrade ZA. Schistosomiasis and liver fibrosis. Parasite Immunol. 2009; 31: 656-663.

2. Pearce EJ, MacDonald AS. The immunobiology of schistosomiasis. Nat Rev Immunol. 2002; 2: 499-511.

3. Brown GW, O’Brien W. Schistosoma mansoni infection with portal hypertension (Symmers’ fibrosis). Proc R Soc Med. 1974; 67: 1027- 1028.

4. Fallon PG. Immunopathology of schistosomiasis: a cautionary tale of mice and men. Immunol. Today. 2000; 21: 29-35.

5. Borojevic R. Experimental murine Schistosomiasis mansoni: establishment of the chronic phase of the disease. Mem. Inst. Oswaldo Cruz. 1992; 87, 171-174.

6. Burke ML, McManus DP, Ramm GA, Duke M, Li Y, Jones MK, et al. Temporal expression of chemokines dictates the hepatic inflammatory infiltrate in a murine model of schistosomiasis. PLoS Negl Trop Dis. 2010; 4: e598.

7. Anthony BJ, Ramm GA, McManus DP. Role of resident liver cells in the pathogenesis of schistosomiasis. Trends Parasitol. 2012; 28: 572-579.

8. de Jesus AR, Silva A, Santana LB, Magalhães A, de Jesus AA, de Almeida RP, et al. Clinical and immunologic evaluation of 31 patients with acute schistosomiasis mansoni. J Infect Dis. 2002; 185: 98-105.

9. Karlmark KR, Tacke F, Dunay IR. Monocytes in health and disease - Minireview. Eur J Microbiol Immunol (Bp). 2012; 2: 97-102.

10. Lopes LM, Pereira MA, Gerken SE, Vaz N. Polyclonal activation of B lymphocytes during experimental infection with Schistosoma mansoni. Parasitology. 1990; 100, 83-91.

11. el-Cheikh MC, Dutra HS, Minóprio P, Borojevic R. Increase of B-lymphocyte number and activity during experimental murine schistosomiasis mansoni. Braz J Med Biol Res. 1994; 27: 1605-1617.

12. Nyame AK, Lewis FA, Doughty BL, Correa-Oliveira R, Cummings RD. Immunity to schistosomiasis: glycans are potential antigenic targets for immune intervention. Exp Parasitol. 2003; 104: 1-13.

13. Van den Berg TK, Honing H, Franke N, van Remoortere A, Schiphorst WE, Liu FT, et al. LacDiNAc-glycans constitute a parasite pattern for galectin-3-mediated immune recognition. J Immunol. 2004; 173: 1902-1907.

14. Vasta GR. Roles of galectins in infection. Nat Rev Microbiol. 2009; 7: 424-438.

15. Oliveira FL, Frazao P, Chammas R, Hsu DK, Liu FT, Borojevic Radovan, et al. Kinetics of mobilization and differentiation of lymphohematopoietic cells during experimental murine schistosomiasis in galectin-3(-/-) mice. J Leukocyte Biol. 2007; 82: 300-310.

16. Oliveira FL, Brand C, Paula AA, Arcanjo KD, Hsu DK, Lui FT, et al. Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of Schistosoma mansoni infection. PLoS One. 2011; 6: e19216.

17. Brand C, Oliveira FL, Ricon L, Fermino ML, Boldrini LC, Hsu DK, et al. The bone marrow compartment is modified in the absence of galectin-3. Cell Tissue Res. 2011; 346: 427-437.

18. Oliveira FL, Bernardes ES, Brand C, Santos SN, Cabanel MP, Arcanjo KD, et al. Lack of galectin-3 up-regulates IgA expression by peritoneal B1 lymphocytes during B cell differentiation. Cell Tissue Res. 2016; 363: 411-426.

19. Carlow DA, Gold MR, Ziltener HJ. Lymphocytes in the peritoneum home to the omentum and are activated by resident dendritic cells. J Immunol. 2009; 183:1155-1165.

20. Lenzi HL, Oliveira DN, Pelajo-Machado M, Borojevic R, Lenzi JA. Coelom-associated lymphomyeloid tissue (milky spots):site of lymphoid and myelomonocytic cell generation. Braz J Med Biol Res. 1996; 29: 19-24.

21. Panasco MS, Pelajo-Machado M, Lenzi HL. Omental and pleural milky spots: different reactivity patterns in mice infected with Schistosoma mansoni reveals coelomic compartmentalisation. Mem Inst Oswaldo Cruz. 2010; 105: 440-444.

22. Oliveira F, Aguiar A, Borojevic R, El-Cheikh M. IgE expression on the surface of B1 and B2 lymphocytes in experimental murine schistosomiasis. Braz J Med Biol Res. 2005; 38: 1033-1042.

23. Beall MJ, Pearce EJ. Human transforming growth factor-β activates a receptor serine/threonine kinase from the intravascular parasite Schistosoma mansoni. J Biol Chem. 2001; 276: 31613-31619.

24. Henderson NC, Mackinnon AC, Farnworth SL, Poirier F, Russo FP, Iredale JP, et al. Galectin-3 regulates myofibroblast activation and hepatic fibrosis. Proc Natl Acad Sci U S A. 2006; 103: 5060-5065.

25. Cortegano I, Pozo V del, Cárdaba B, Andrés B de, Gallardo S, Amo A del, et al. Galectin-3 down-regulates IL-5 gene expression on different cell types. J Immunol. 1998; 161: 385-389. 26.Cerutti A, Rescigno M. The biology of intestinal immunoglobulin A responses. Immunity. 2008; 28: 740-750.

27. Merluzzi S, Frossi B, Gri G, Parusso S, Tripodo C, Pucillo C. Mast cells enhance proliferation of B lymphocytes and drive their differentiation toward IgA-secreting plasma cells. Blood. 2010; 115: 2810-2817.

28. Dent LA, Daly C, Geddes A, Cormie J, Finlay DA, Bignold L, et al. Immune responses of IL-5 transgenic mice to parasites and aeroallergens. Mem Inst Oswaldo Cruz. 1997; 92: 45-54.

29. Swartz JM, Dyer KD, Cheever AW, Ramalingam T, Pesnicak L, Domachowske JB, et al. Schistosoma mansoni infection in eosinophil lineage-ablated mice. Blood. 2006; 108: 2420-2427.

30. Reiman RM, Thompson RW, Feng CG, Hari D, Knight R, Cheever AW, et al. Interleukin-5 (IL-5) augments the progression of liver fibrosis by regulating IL-13 activity. Infect Immun. 2006; 74: 1471-1479.

31. Jacobs W, Kumar-Singh S, Bogers J, Van de Vijver K, Deelder A, Van Marck E. Transforming growth factor-beta, basement membrane components and heparan sulphate proteoglycans in experimental hepatic schistosomiasis mansoni. Cell Tissue Res. 1998; 292: 101-106.

32. Kaviratne M, Hesse M, Leusink M, Cheever AW, Davies SJ, McKerrow JH, et al. IL-13 activates a mechanism of tissue fibrosis that is completely TGF-beta independent. J Immunol. 2004; 173: 4020-4029.

33. Freitas TC, Jung E, Pearce EJ. TGF-beta signaling controls embryo development in the parasitic flatworm Schistosoma mansoni. PLoS Pathog. 2007; 3: e52.

34. Attia YM, Elalkamy EF, Hammam OA, Mahmoud SS, El-Khatib AS. Telmisartan, an AT1 receptor blocker and a PPAR gamma activator, alleviates liver fibrosis induced experimentally by Schistosoma mansoni infection. Parasit Vectors. 2013; 6: 199.

35. Said E, Said SA, Elkashef WF, Gameil NM, Ammar EM. Tranilast ameliorates impaired hepatic functions in Schistosoma mansoniinfected mice. Inflammopharmacology. 2012; 20: 77-87.

36. Paiva LA, Maya-Monteiro CM, Bandeira-Melo C, Silva PM, ElCheikh MC, Teodoro AJ, et al. Interplay of cysteinyl leukotrienes and TGF-β in the activation of hepatic stellate cells from Schistosoma mansoni granulomas. Biochim Biophys Acta. 2010; 1801: 1341-1348.

37. Paiva LA, Coelho KA, Luna-Gomes T, El-Cheikh MC, Borojevic R, Perez SA, et al. Schistosome infection-derived Hepatic Stellate Cells are cellular source of prostaglandin D?: role in TGF-β-stimulated VEGF production. Prostaglandins Leukot Essent Fatty Acids. 2015; 95: 57- 62.

38. Paiva LA, Brand C, Bandeira-Melo C, Bozza PT, El-Cheikh MC, Silva PM, et al. Hepatic myofibroblasts derived from Schistosoma mansoniinfected mice are a source of IL-5 and eotaxin: controls of eosinophil populations in vitro. Parasit Vectors. 2015; 8: 577

39. Maeda N, Kawada N, Seki S, Arakawa T, Ikeda K, Iwao H, et al. Stimulation of proliferation of rat hepatic stellate cells by galectin-1 and galectin-3 through different intracellular signaling pathways. J Biol Chem. 2003; 278: 18938-18944.

40. Jiang JX, Chen X, Hsu DK, Baghy K, Serizawa N, Scott F, et al. Galectin-3 modulates phagocytosis-induced stellate cell activation and liver fibrosis in vivo. Am J Physiol Gastrointest Liver Physiol. 2012; 302: G439-446.

41. Oliveira FL, Carneiro K, Brito JM, Cabanel M, Pereira JX, Paiva LA, et al. Galectin-3, histone deacetylases, and Hedgehog signaling: Possible convergent targets in schistosomiasis-induced liver fibrosis. PLoS Negl Trop Dis. 2017; 11: e0005137.

Received : 14 Jun 2016
Accepted : 07 Mar 2016
Published : 09 Mar 2016
Annals of Otolaryngology and Rhinology
ISSN : 2379-948X
Launched : 2014
JSM Schizophrenia
Launched : 2016
Journal of Nausea
Launched : 2020
JSM Internal Medicine
Launched : 2016
JSM Hepatitis
Launched : 2016
JSM Oro Facial Surgeries
ISSN : 2578-3211
Launched : 2016
Journal of Human Nutrition and Food Science
ISSN : 2333-6706
Launched : 2013
JSM Regenerative Medicine and Bioengineering
ISSN : 2379-0490
Launched : 2013
JSM Spine
ISSN : 2578-3181
Launched : 2016
Archives of Palliative Care
ISSN : 2573-1165
Launched : 2016
JSM Nutritional Disorders
ISSN : 2578-3203
Launched : 2017
Annals of Neurodegenerative Disorders
ISSN : 2476-2032
Launched : 2016
Journal of Fever
ISSN : 2641-7782
Launched : 2017
JSM Bone Marrow Research
ISSN : 2578-3351
Launched : 2016
JSM Mathematics and Statistics
ISSN : 2578-3173
Launched : 2014
Journal of Autoimmunity and Research
ISSN : 2573-1173
Launched : 2014
JSM Arthritis
ISSN : 2475-9155
Launched : 2016
JSM Head and Neck Cancer-Cases and Reviews
ISSN : 2573-1610
Launched : 2016
JSM General Surgery Cases and Images
ISSN : 2573-1564
Launched : 2016
JSM Anatomy and Physiology
ISSN : 2573-1262
Launched : 2016
JSM Dental Surgery
ISSN : 2573-1548
Launched : 2016
Annals of Emergency Surgery
ISSN : 2573-1017
Launched : 2016
Annals of Mens Health and Wellness
ISSN : 2641-7707
Launched : 2017
Journal of Preventive Medicine and Health Care
ISSN : 2576-0084
Launched : 2018
Journal of Chronic Diseases and Management
ISSN : 2573-1300
Launched : 2016
Annals of Vaccines and Immunization
ISSN : 2378-9379
Launched : 2014
JSM Heart Surgery Cases and Images
ISSN : 2578-3157
Launched : 2016
Annals of Reproductive Medicine and Treatment
ISSN : 2573-1092
Launched : 2016
JSM Brain Science
ISSN : 2573-1289
Launched : 2016
JSM Biomarkers
ISSN : 2578-3815
Launched : 2014
JSM Biology
ISSN : 2475-9392
Launched : 2016
Archives of Stem Cell and Research
ISSN : 2578-3580
Launched : 2014
Annals of Clinical and Medical Microbiology
ISSN : 2578-3629
Launched : 2014
JSM Pediatric Surgery
ISSN : 2578-3149
Launched : 2017
Journal of Memory Disorder and Rehabilitation
ISSN : 2578-319X
Launched : 2016
JSM Head and Face Medicine
ISSN : 2578-3793
Launched : 2016
JSM Cardiothoracic Surgery
ISSN : 2573-1297
Launched : 2016
JSM Bone and Joint Diseases
ISSN : 2578-3351
Launched : 2017
JSM Bioavailability and Bioequivalence
ISSN : 2641-7812
Launched : 2017
JSM Atherosclerosis
ISSN : 2573-1270
Launched : 2016
Journal of Genitourinary Disorders
ISSN : 2641-7790
Launched : 2017
Journal of Fractures and Sprains
ISSN : 2578-3831
Launched : 2016
Journal of Autism and Epilepsy
ISSN : 2641-7774
Launched : 2016
Annals of Marine Biology and Research
ISSN : 2573-105X
Launched : 2014
JSM Health Education & Primary Health Care
ISSN : 2578-3777
Launched : 2016
JSM Communication Disorders
ISSN : 2578-3807
Launched : 2016
Annals of Musculoskeletal Disorders
ISSN : 2578-3599
Launched : 2016
Annals of Virology and Research
ISSN : 2573-1122
Launched : 2014
JSM Renal Medicine
ISSN : 2573-1637
Launched : 2016
Journal of Muscle Health
ISSN : 2578-3823
Launched : 2016
JSM Genetics and Genomics
ISSN : 2334-1823
Launched : 2013
JSM Anxiety and Depression
ISSN : 2475-9139
Launched : 2016
Clinical Journal of Heart Diseases
ISSN : 2641-7766
Launched : 2016
Annals of Medicinal Chemistry and Research
ISSN : 2378-9336
Launched : 2014
JSM Pain and Management
ISSN : 2578-3378
Launched : 2016
JSM Women's Health
ISSN : 2578-3696
Launched : 2016
Clinical Research in HIV or AIDS
ISSN : 2374-0094
Launched : 2013
Journal of Endocrinology, Diabetes and Obesity
ISSN : 2333-6692
Launched : 2013
Journal of Substance Abuse and Alcoholism
ISSN : 2373-9363
Launched : 2013
JSM Neurosurgery and Spine
ISSN : 2373-9479
Launched : 2013
Journal of Liver and Clinical Research
ISSN : 2379-0830
Launched : 2014
Journal of Drug Design and Research
ISSN : 2379-089X
Launched : 2014
JSM Clinical Oncology and Research
ISSN : 2373-938X
Launched : 2013
JSM Bioinformatics, Genomics and Proteomics
ISSN : 2576-1102
Launched : 2014
JSM Chemistry
ISSN : 2334-1831
Launched : 2013
Journal of Trauma and Care
ISSN : 2573-1246
Launched : 2014
JSM Surgical Oncology and Research
ISSN : 2578-3688
Launched : 2016
Annals of Food Processing and Preservation
ISSN : 2573-1033
Launched : 2016
Journal of Radiology and Radiation Therapy
ISSN : 2333-7095
Launched : 2013
JSM Physical Medicine and Rehabilitation
ISSN : 2578-3572
Launched : 2016
Annals of Clinical Pathology
ISSN : 2373-9282
Launched : 2013
Annals of Cardiovascular Diseases
ISSN : 2641-7731
Launched : 2016
Journal of Behavior
ISSN : 2576-0076
Launched : 2016
Annals of Clinical and Experimental Metabolism
ISSN : 2572-2492
Launched : 2016
Clinical Research in Infectious Diseases
ISSN : 2379-0636
Launched : 2013
JSM Microbiology
ISSN : 2333-6455
Launched : 2013
Journal of Urology and Research
ISSN : 2379-951X
Launched : 2014
Journal of Family Medicine and Community Health
ISSN : 2379-0547
Launched : 2013
Annals of Pregnancy and Care
ISSN : 2578-336X
Launched : 2017
JSM Cell and Developmental Biology
ISSN : 2379-061X
Launched : 2013
Annals of Aquaculture and Research
ISSN : 2379-0881
Launched : 2014
Clinical Research in Pulmonology
ISSN : 2333-6625
Launched : 2013
Journal of Immunology and Clinical Research
ISSN : 2333-6714
Launched : 2013
Annals of Forensic Research and Analysis
ISSN : 2378-9476
Launched : 2014
JSM Biochemistry and Molecular Biology
ISSN : 2333-7109
Launched : 2013
Annals of Breast Cancer Research
ISSN : 2641-7685
Launched : 2016
Annals of Gerontology and Geriatric Research
ISSN : 2378-9409
Launched : 2014
Journal of Sleep Medicine and Disorders
ISSN : 2379-0822
Launched : 2014
JSM Burns and Trauma
ISSN : 2475-9406
Launched : 2016
Chemical Engineering and Process Techniques
ISSN : 2333-6633
Launched : 2013
Annals of Clinical Cytology and Pathology
ISSN : 2475-9430
Launched : 2014
JSM Allergy and Asthma
ISSN : 2573-1254
Launched : 2016
Journal of Neurological Disorders and Stroke
ISSN : 2334-2307
Launched : 2013
Annals of Sports Medicine and Research
ISSN : 2379-0571
Launched : 2014
JSM Sexual Medicine
ISSN : 2578-3718
Launched : 2016
Annals of Vascular Medicine and Research
ISSN : 2378-9344
Launched : 2014
JSM Biotechnology and Biomedical Engineering
ISSN : 2333-7117
Launched : 2013
Journal of Hematology and Transfusion
ISSN : 2333-6684
Launched : 2013
JSM Environmental Science and Ecology
ISSN : 2333-7141
Launched : 2013
Journal of Cardiology and Clinical Research
ISSN : 2333-6676
Launched : 2013
JSM Nanotechnology and Nanomedicine
ISSN : 2334-1815
Launched : 2013
Journal of Ear, Nose and Throat Disorders
ISSN : 2475-9473
Launched : 2016
JSM Ophthalmology
ISSN : 2333-6447
Launched : 2013
Journal of Pharmacology and Clinical Toxicology
ISSN : 2333-7079
Launched : 2013
Annals of Psychiatry and Mental Health
ISSN : 2374-0124
Launched : 2013
Medical Journal of Obstetrics and Gynecology
ISSN : 2333-6439
Launched : 2013
Annals of Pediatrics and Child Health
ISSN : 2373-9312
Launched : 2013
JSM Clinical Pharmaceutics
ISSN : 2379-9498
Launched : 2014
JSM Foot and Ankle
ISSN : 2475-9112
Launched : 2016
JSM Alzheimer's Disease and Related Dementia
ISSN : 2378-9565
Launched : 2014
Journal of Addiction Medicine and Therapy
ISSN : 2333-665X
Launched : 2013
Journal of Veterinary Medicine and Research
ISSN : 2378-931X
Launched : 2013
Annals of Public Health and Research
ISSN : 2378-9328
Launched : 2014
Annals of Orthopedics and Rheumatology
ISSN : 2373-9290
Launched : 2013
Journal of Clinical Nephrology and Research
ISSN : 2379-0652
Launched : 2014
Annals of Community Medicine and Practice
ISSN : 2475-9465
Launched : 2014
Annals of Biometrics and Biostatistics
ISSN : 2374-0116
Launched : 2013
JSM Clinical Case Reports
ISSN : 2373-9819
Launched : 2013
Journal of Cancer Biology and Research
ISSN : 2373-9436
Launched : 2013
Journal of Surgery and Transplantation Science
ISSN : 2379-0911
Launched : 2013
Journal of Dermatology and Clinical Research
ISSN : 2373-9371
Launched : 2013
JSM Gastroenterology and Hepatology
ISSN : 2373-9487
Launched : 2013
Annals of Nursing and Practice
ISSN : 2379-9501
Launched : 2014
JSM Dentistry
ISSN : 2333-7133
Launched : 2013
Author Information X