Induction of IL‐1, in the Testes of Adult Mice, Following Subcutaneous Administration of Turpentine

Elhija, Mahmoud Abu; Lunenfeld, Eitan; Huleihel, Mahmoud

doi:10.1111/j.1600-0897.2005.00344.x

Cited by 4 publications

(3 citation statements)

References 41 publications

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“…It is also interesting to note that IL-1ß levels were found to be reduced in human testicular sections with impaired spermatogenesis [ 47 , 56 ]. It has been suggested that this was somehow related to Leydig cell apoptosis [ 47 , 57 , 58 ]. In this context, homeostasis of the testicular IL-1ß pathway could regulate androgen production and consequently spermatogenesis [ 59 ].…”

Section: Methodsmentioning

confidence: 99%

The NLRP3 inflammasome: molecular activation and regulation in spermatogenesis and male infertility; a systematic review

Tavalaee

Rahmani

Drevet

et al. 2022

Basic Clin. Androl.

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Background Infertility related to varicocele, infections, metabolic dysfunctions, oxidative stress and environmental toxicants is also associated with inflammatory processes that ultimately lead to the activation of the inflammasome pathway (IP). IP is classically activated by DAMPs, MAMPs or LAMPs, which stand for Damage-, Microbe- or Lifestyle-Associated Molecular Patterns, respectively. The most important player in IP activation is the NLRP3 (NOD[Nuclear oligomerization domain]-, LRR[Leucine rich repeat]- and pyrin domain-containing protein 3) which functions as an intracellular sensor of D/M/L-AMPs resulting in activation of caspase-1, promotion of apoptosis, pyroptosis and generation of inflammatory cytokines. This review addresses the question of whether IP activation might be associated with male infertility situations. Results & conclusions We conducted a systematic review of articles published in the Google Scholar, and PubMed databases through October 2021. It turns out that inflammasome activation and its consequences including cytokine storms, apoptosis and pyroptosis could be associated with the reduced sperm count as well as the structural and functional sperm defects recorded in several situations associated with male infertility suggesting that anti-inflammatory therapeutic strategies could be possibly considered to restore male fertility in future research.

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Section: Methodsmentioning

confidence: 99%

The NLRP3 inflammasome: molecular activation and regulation in spermatogenesis and male infertility; a systematic review

Tavalaee

Rahmani

Drevet

et al. 2022

Basic Clin. Androl.

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“…Serum IL-6 and IL-1 are high during this early phase, whereas serum TNFa does not play a role. Five days after turpentine serum IL-1 and IL-6 decrease, temperature and food-intake return to normal and mice recover, although liver Il1b mRNA increases which is characteristic for the development of a systemic acute phase response (Boelen et al 1996, 2005, Leon 2002, Elhija et al 2006.…”

Section: Discussionmentioning

confidence: 99%

Skeletal muscle deiodinase type 2 regulation during illness in mice

Kwakkel¹,

Beeren²,

Ackermans³

et al. 2009

Journal of Endocrinology

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We have previously shown that skeletal muscle deiodinase type 2 (D2) mRNA (listed as Dio2 in MGI Database) is upregulated in an animal model of acute illness. However, human studies on the expression of muscle D2 during illness report conflicting data. Therefore, we evaluated the expression of skeletal muscle D2 and D2-regulating factors in two mouse models of illness that differ in timing and severity of illness: 1) turpentine-induced inflammation, and 2) Streptococcus pneumoniae infection. During turpentineinduced inflammation, D2 mRNA and activity increased compared to pair-fed controls, most prominently at day 1 and 2, whereas after S. pneumoniae infection D2 mRNA decreased. We evaluated the association of D2 expression with serum thyroid hormones, (de-)ubiquitinating enzymes ubiquitin-specific peptidase 33 and WD repeat and SOCS box-containing 1 (Wsb1), cytokine expression and activation of inflammatory pathways and cAMP pathway.During chronic inflammation the increased muscle D2 expression is associated with the activation of the cAMP pathway. The normalization of D2 5 days after turpentine injection coincides with increased Wsb1 and tumor necrosis factor a expression. Muscle interleukin-1b (Il1b) expression correlated with decreased D2 mRNA expression after S. pneumoniae infection. In conclusion, muscle D2 expression is differentially regulated during illness, probably related to differences in the inflammatory response and type of pathology. D2 mRNA and activity increases in skeletal muscle during the acute phase of chronic inflammation compared to pair-fed controls probably due to activation of the cAMP pathway. In contrast, muscle D2 mRNA decreases 48 h after a severe bacterial infection, which is associated with local Il1b mRNA expression and might also be due to diminished food-intake.

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“…It is known that the increased expression of these proinflammatory cytokines results in testicular dysfunction [36]. Models of acute inflammation by injection of turpentine [37] and experimental varicocele [38] increased protein or mRNA levels of both IL-1α and IL-1β in the testis. However, the kinetics of testicular IL-1 in EAO have not yet been reported.…”

Section: Discussionmentioning

confidence: 99%

Intratesticular Expression of mRNAs of Both Interferon γ and Tumor Necrosis Factor α is Significantly Increased in Experimental Autoimmune Orchitis in Mice

Terayama

Naito

et al. 2011

Journal of Reproduction and Development

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Abstract. Experimental autoimmune orchitis (EAO) is one of the models of immunological male infertility. Murine EAO is CD4+T cell-dependent and classically induced by immunization with a testicular homogenate and adjuvants. We previously established that immunization with viable syngeneic testicular germ cells (TGC) can also induce murine EAO with no use of any adjuvant. Analyses of this EAO model have already revealed that cultured spleen cells of immunized mice secreted interferon (IFN)-γ and that treatment of the immunized mice with anti-IFN-γ monoclonal antibodies significantly suppressed the EAO. It is known that both IFN-γ and tumor necrosis factor (TNF)-α are representative cytokines of Th1 cells and exhibit local toxicity toward the seminiferous epithelium in vivo. However, changes in these two cytokines in EAO-affected testes have not yet been investigated. Therefore, in the present study, we investigated the expression of intratesticular IFN-γ and TNF-α mRNAs in TGC-induced EAO using real-time RT-PCR. The results demonstrated that the intratesticular mRNAs for both IFN-γ and TNF-α significantly increased, while other cytokines such as IL-1α, IL-1β, IL-6 and TGF-β did not show dramatic changes in the immunized mice. These results suggest that secretion of significant amounts of IFN-γ and TNF-α in situ contributes to the spermatogenic disturbance in EAO. Key words: Autoimmunity, Cytokine, Spermatogenic disturbance, Testis (J. Reprod. Dev. 57: [296][297][298][299][300][301][302] 2011) xperimental autoimmune orchitis (EAO) is a model of immunologic inflammation leading to male infertility [1]. The histopathology is characterized by intratesticular infiltration of CD4+T cells, CD8+T cells, B cells and plasma cells, followed by spermatogenic disturbance [2,3]. Classically, immunization with a testicular homogenate (TH) emulsified in complete Freund's adjuvant (CFA) followed by intravenous injections of Bordetella pertussis (BP) is necessary for induction of EAO in mice [4,5]. TH+CFA+BP-induced EAO in mice is dependent on CD4+ T cells that secrete tumor necrosis factor (TNF)-α and interferon (IFN)-γ in vitro [6]. It has also been reported that the disease can be suppressed in vivo by the administration of anti-TNF-α antibodies but not anti-IFN-γ antibodies [6]. In rat EAO induced by immunization with TH+CFA+BP, it was shown that isolated testicular macrophages secreted both . However, the intratesticular changes in IFN-γ and TNF-α mRNA expression at the organ level have not yet been investigated in any EAO model.We previously established that two subcutaneous injections of viable syngeneic testicular germ cells (TGC) can induce CD4+ T cell-dependent EAO in both A/J and C3H/He mice with a very high incidence [2,10]. This model is unique in that CFA and BP are not necessary for EAO induction. However, in spite of no use of these adjuvants, it was found that delayed type hypersensitivity rather than humoral immunity against TGC antigens is critical for induction of the disease [2,11,12]. It was also shown tha...

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Induction of IL‐1, in the Testes of Adult Mice, Following Subcutaneous Administration of Turpentine

Cited by 4 publications

References 41 publications

The NLRP3 inflammasome: molecular activation and regulation in spermatogenesis and male infertility; a systematic review

The NLRP3 inflammasome: molecular activation and regulation in spermatogenesis and male infertility; a systematic review

Skeletal muscle deiodinase type 2 regulation during illness in mice

Intratesticular Expression of mRNAs of Both Interferon γ and Tumor Necrosis Factor α is Significantly Increased in Experimental Autoimmune Orchitis in Mice

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Induction of IL‐1, in the Testes of Adult Mice, Following Subcutaneous Administration of Turpentine

Cited by 4 publications

References 41 publications

The NLRP3 inflammasome: molecular activation and regulation in spermatogenesis and male infertility; a systematic review

The NLRP3 inflammasome: molecular activation and regulation in spermatogenesis and male infertility; a systematic review

Skeletal muscle deiodinase type 2 regulation during illness in mice

Intratesticular Expression of mRNAs of Both Interferon &gamma; and Tumor Necrosis Factor &alpha; is Significantly Increased in Experimental Autoimmune Orchitis in Mice

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Intratesticular Expression of mRNAs of Both Interferon γ and Tumor Necrosis Factor α is Significantly Increased in Experimental Autoimmune Orchitis in Mice