Cytokine profiles in the testes of rats treated with lipopolysaccharide reveal localized suppression of inflammatory responses

O'Bryan, Moira K; Gerdprasert, Orapin; Nikolic-Paterson, David J.; Meinhardt, Andreas; Muir, Julie A.; Foulds, Lynda M.; Phillips, David J.; Kretser, David Morritz de; Hedger, Mark P.

doi:10.1152/ajpregu.00651.2004

Cited by 83 publications

(87 citation statements)

References 73 publications

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“…IL-10 can be induced by orchitis and is predominantly produced by testicular macrophages. 93 Overexpression of IL-10 in the testis significantly reduces the levels of inflammation in EAO models. 94 Therefore, multiple immunosuppressive factors are involved in the maintenance of immune homeostasis in testicular tissue.…”

Section: Immune Privilege In the Testismentioning

confidence: 99%

Testicular defense systems: immune privilege and innate immunity

et al. 2014

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The mammalian testis possesses a special immunological environment because of its properties of remarkable immune privilege and effective local innate immunity. Testicular immune privilege protects immunogenic germ cells from systemic immune attack, and local innate immunity is important in preventing testicular microbial infections. The breakdown of local testicular immune homeostasis may lead to orchitis, an etiological factor of male infertility. The mechanisms underlying testicular immune privilege have been investigated for a long time. Increasing evidence shows that both a local immunosuppressive milieu and systemic immune tolerance are involved in maintaining testicular immune privilege status. The mechanisms underlying testicular innate immunity are emerging based on the investigation of the pattern recognition receptor-mediated innate immune response in testicular cells. This review summarizes our current understanding of testicular defense mechanisms and identifies topics that merit further investigation.

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Section: Immune Privilege In the Testismentioning

confidence: 99%

Testicular defense systems: immune privilege and innate immunity

et al. 2014

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“…Both forms of IL-1 bind to the same receptor with the same range of biological actions, including the stimulation of activin A production by Sertoli cells, and are inhibited by IL-1ra (Okuma et al 2005a(Okuma et al , 2005b. Inflammation in the testis involves production of both IL-1 forms (O'Bryan et al 2005, Okuma et al 2005b. Rather than duplicating these studies using both forms of IL-1, however, IL-1b was employed as the bioactive ligand for all the studies described herein.…”

Section: Introductionmentioning

confidence: 99%

Regulated production of activin A and inhibin B throughout the cycle of the seminiferous epithelium in the rat

Okuma

O’Connor

Hayashi

et al. 2006

Journal of Endocrinology

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Production and regulation of activin A and inhibin B during the cycle of the seminiferous epithelium were investigated in adult rats. Immunohistochemistry localised the activin b Asubunit to the Sertoli cell cytoplasm, with much weaker expression in spermatocytes and spermatids. Both activin A and inhibin B, measured by ELISA were secreted by, seminiferous tubule fragments over 72 h in culture. Activin A was secreted in a cyclic manner with peak secretion from tubules isolated at stage VIII. Tubules collected during stage VI produced the least activin A. Inhibin B secretion was highest from stage IX-I tubules and lowest from stage VII tubules. Addition of interleukin-1b (IL-1b) had relatively little effect on activin A or inhibin B secretion in culture. In contrast, the peak secretion of activin A by stage VIII tubules was blocked by co-incubation with an excess of human recombinant IL-1 receptor antagonist, whereas inhibin B secretion increased slightly. Dibutyryl cAMP stimulated activin A secretion by late stage VII and VIII tubules and stimulated inhibin B across all stages. These data indicate that activin A and inhibin B are cyclically regulated within the seminiferous epithelium, with endogenous IL-1 (presumably IL-1a produced by the Sertoli cells), responsible for a peak of activin A production subsequent to sperm release at stage VIII. These data provide direct evidence that production of activin A and inhibin B by the Sertoli cell is locally modulated by IL-1a, in addition to FSH/cAMP, under the influence of the developing spermatogenic cells.

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“…Studies have shown that administration of lipopolysaccharide (LPS), a potent inflammatory stimulus from the cell wall of gram-negative bacteria, provides a useful model for investigating this process in vivo and in vitro (Wallgren et al 1989, Hales 1992, Jonsson et al 2001, O'Bryan et al 2005.…”

Section: Introductionmentioning

confidence: 99%

“…The production of both cytokines by the Sertoli cells is stimulated by the developing germ cells and residual bodies (Gérard et al 1992, Jonsson et al 1999, and both cytokines have been implicated in the control of spermatogonial and spermatocyte development , Hakovirta et al 1995. Expression of IL-1 in the normal testis is relatively low, but this cytokine is up-regulated during inflammation due to production by testicular macrophages and Leydig cells (Gow et al 2001, Jonsson et al 2001, O'Bryan et al 2005. Testicular production of IL-6 also increases during inflammation in adult rats (O'Bryan et al 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Expression of IL-1 in the normal testis is relatively low, but this cytokine is up-regulated during inflammation due to production by testicular macrophages and Leydig cells (Gow et al 2001, Jonsson et al 2001, O'Bryan et al 2005. Testicular production of IL-6 also increases during inflammation in adult rats (O'Bryan et al 2005). The response of testicular IL-1 to inflammation is less clear.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of activin A and inhibin B secretion by inflammatory mediators in adult rat Sertoli cell cultures

Okuma¹,

O’Connor²,

Muir³

et al. 2005

Journal of Endocrinology

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The regulation of Sertoli cell activin A and inhibin B secretion during inflammation was investigated in vitro. Adult rat Sertoli cells were incubated with the inflammatory mediators, lipopolysaccharide (LPS), interleukin-1 (IL-1 ), IL-6 and the IL-1 receptor antagonist (IL-1ra) over 48 h in culture. Activin A, inhibin B and IL-1 were measured in the culture medium by specific two-site ELISAs. Both IL-1 -and LPS-stimulated activin A and inhibited inhibin B secretion. LPS also stimulated the production of IL-1 in the cultures. In contrast to IL-1 , IL-6 had no effect on activin A, although it did have a significant inhibitory effect on inhibin B secretion. Ovine follicle-stimulating hormone (FSH) and the cAMP analogue dibutyryl cAMP opposed the actions of IL-1 and LPS by suppressing activin A and IL-1 secretion and by stimulating inhibin B. Blocking IL-1 activity in the cultures by addition of an excess of IL-1ra completely prevented the response of activin A to exogenous IL-1 , and reduced the response to LPS by 50%. In the presence of IL-1ra, basal secretion of inhibin B was increased, but IL-1ra was unable to reverse the suppression of inhibin B by LPS. These data indicate the importance of both IL-1 isoforms in regulating secretion of activin A and inhibin B by mature Sertoli cells during inflammation. The data also establish that inflammation exerts its effects on activin A and inhibin B secretion via other pathways in addition to those mediated by IL-1, and that hormonal stimulation by FSH and cAMP moderates the Sertoli cell response to inflammation. Interference with the complex interactions between these cytokines and hormones may contribute to the disruption of reproductive function that can accompany infection and illness in men.

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Cytokine profiles in the testes of rats treated with lipopolysaccharide reveal localized suppression of inflammatory responses

Abstract: Cytokine profiles in the testes of rats treated with lipopolysaccharide reveal localized suppression of inflammatory responses.

Cited by 83 publications

References 73 publications

Testicular defense systems: immune privilege and innate immunity

Testicular defense systems: immune privilege and innate immunity

Regulated production of activin A and inhibin B throughout the cycle of the seminiferous epithelium in the rat

Regulation of activin A and inhibin B secretion by inflammatory mediators in adult rat Sertoli cell cultures

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