ORIGINAL ARTICLE: Identification of Toll‐Like Receptors in the Rat (Rattus norvegicus): Messenger RNA Expression in the Male Reproductive Tract Under Conditions of Androgen Variation

Biswas, Barnali; Narmadha, Ganapathy; Choudhary, M. Iqbal; French, Frank S.; Hall, Susan H.; Yenugu, Suresh

doi:10.1111/j.1600-0897.2009.00732.x

Cited by 10 publications

(6 citation statements)

References 29 publications

(54 reference statements)

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“…784 In rat seminal vesicles, mRNA for TLR2, 5,6,7,8,9,10, and 11 were highly expressed, with low levels of the remaining TLRs. 776 Notably, expression of CD14 was higher in the prostate and seminal vesicles of the rat than in any other tissue of the male reproductive tract. 443 Studies have shown that sequence variants in TLR4 and the TLR1-TLR6-TLR10 gene cluster in the human are associated with an increased risk of prostate cancer, suggesting a link between susceptibility to inflammation and tumorigenesis in this organ.…”

Section: Production and Actions Of Inflammatory Mediatorsmentioning

confidence: 93%

“…The TLRs are found throughout the epithelium, and in immune cells, of the posttesticular reproductive tract. 109,[441][442][443][444]776 Studies in the rat and mouse have produced some conflicting data, but overall indicate that expression levels of TLR1-6 in the epididymis are similar to those found in the testis, with expression progressively declining toward the vas deferens. On the other hand, expression of TLRs 7, 9, and 11 tends to be higher in the epididymis and vas deferens than in the testis (Table 19.4).…”

Section: Production and Actions Of Inflammatory Mediatorsmentioning

confidence: 99%

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The Immunophysiology of Male Reproduction

Hedger

2015

Knobil and Neill's Physiology of Reproduction

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Section: Production and Actions Of Inflammatory Mediatorsmentioning

confidence: 93%

Section: Production and Actions Of Inflammatory Mediatorsmentioning

confidence: 99%

The Immunophysiology of Male Reproduction

Hedger

2015

Knobil and Neill's Physiology of Reproduction

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“…Signalling pathways effected by these receptors promote the production of antimicrobial proteins and peptides, and these processes are well characterised in reproductive and in other organ systems (Mukherjee, Karmakar, & Babu, ). We and other groups demonstrated the abundant expression of Tlr1‐13 in the male reproductive tract of different species (Biswas et al, ; Biswas & Yenugu, ; Liman, Alan, & Apaydin, ; Palladino, Johnson, Gupta, Chapman, & Ojha, ; Palladino, Savarese, Chapman, Dughi, & Plaska, ; Pioli et al, ). The general gene expression pattern and LPS/uropathogenic Escherichia coli ‐mediated induction of rat Defb s and DEFB‐like proteins and peptides belonging to the Sperm‐Associated Antigen 11 (SPAG11) family were reported in the male reproductive system (Biswas & Yenugu, , , ; Yenugu, Chintalgattu, et al, ; Yenugu, Hamil, French, & Hall, ).…”

Section: Introductionmentioning

confidence: 60%

Tlr1‐13, Nod1/2 and antimicrobial gene expression in the epididymis and testis of rats with alloxan‐induced diabetes

et al. 2019

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Pattern recognition receptors (PRRs) such as toll‐like receptors (TLRs) and nuclear oligomerization domain (NOD) receptors along with antimicrobial proteins and peptides (AMPs) are crucial for innate immunity. The pathology of insulin‐dependent diabetes mellitus is associated with the disrupted expression of TLRs, NODs and AMPs in the kidney, lungs and other organs. However, such a relation in the male reproductive tract is not yet investigated. In this study, we analysed the expression pattern of Tlr1‐13, Nod1/2 receptors and AMPs (β‐defensins and defensin‐like proteins of the Sperm‐Associated Antigen 11 (Spag11) family) in the male reproductive tissues (caput, cauda and testis) obtained from diabetic or insulin‐treated diabetic or untreated control rats. Alterations in the expression pattern of Tlr1‐13, Nod 1/ 2, Defb1, 2, 21, 24, 27, 30 and Spag11a/ c/ t were observed under diabetic conditions. Administration of insulin to diabetic rats could modulate the expression pattern of only some these genes. Results of our study indicate perturbed gene expression profile of Tlrs, Nod1/2, Defbs and Spag11 isoforms in the epididymis and testis of diabetic rats, and this could be one of the important reasons for the increased risk of infections in the male genital tract.

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“…The prediction might be helped when genes of TLR11 from more species were analyzed. TLR11 is present in the mouse and rat genomes but not in the genomes of cat, dog, frog, chimp and fugu [ 16 , 41 ]. Thus, we can imagine the evolutionary pressures that cause TLR11 to downgrade to a non-coding gene in humans and certain animals.…”

Section: Discussionmentioning

confidence: 99%

Toxoplasma gondii microneme protein MIC3 induces macrophage TNF-α production and Ly6C expression via TLR11/MyD88 pathway

Qiu

Xie²,

Shao³

et al. 2023

PLoS Negl Trop Dis

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Toxoplasma gondii is the most successful parasite worldwide. It is of great interest to understand how T. gondii induce different immune responses in different hosts. In this study, we found that a peptide of T. gondii microneme protein MIC3 induced TNF-α production, NF-κB phosphorylation, iNOS transcription and Ly6C expression in mouse macrophage RAW264.7 cells. MyD88 inhibition, small interfering RNA against Tlr11 and CRISPR/Cas9-mediated knock-out of Tlr11 all reduced MIC3-induced TNF-α production, NF-κB phosphorylation, iNOS transcription and Ly6C expression. Additionally, we determined the location of MIC3 peptide in mouse macrophages using immunofluorescence. MIC3 could both adhere to the cell membrane of mouse macrophages and enter the cells. These results suggest that MIC3 trigger the immune responses in mouse macrophages via TLR11/MyD88/NF-κB pathway. It is known that human macrophages lacking TLR11. We predicted that the immune responses induced by MIC3 in human macrophages were significantly different from those in mouse macrophages. As expected, MIC3 peptide failed to induce TNF-α expression, iNOS expression and NF-κB phosphorylation in human THP-1 derived macrophages. MIC3 induces macrophage immune responses via TLR11. Intriguingly, the amino acid sequence of MIC3 is completely different from the well-known TLR11 ligand profilin, which generates a potent IL-12p40, TNF-α and IL-6 response. In marked contrast to profilin, MIC3 could not induce IL-12p40 expression in both mouse RAW264.7 cells and human THP-1 derived macrophages. Furthermore, the simulated tertiary structure of MIC3 peptide shows poor similarity with the crystal structure of profilin, suggesting that MIC3 might be a different ligand from profilin. These findings about MIC3 and TLR11 will provide us with important insights into the pathogenesis of toxoplasmosis and coevolution during host-parasite interaction.

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ORIGINAL ARTICLE: Identification of Toll‐Like Receptors in the Rat (Rattus norvegicus): Messenger RNA Expression in the Male Reproductive Tract Under Conditions of Androgen Variation

Cited by 10 publications

References 29 publications

The Immunophysiology of Male Reproduction

The Immunophysiology of Male Reproduction

Tlr1‐13, Nod1/2 and antimicrobial gene expression in the epididymis and testis of rats with alloxan‐induced diabetes

Toxoplasma gondii microneme protein MIC3 induces macrophage TNF-α production and Ly6C expression via TLR11/MyD88 pathway

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