Toll‐like receptor‐4 deficiency inhibits ultraviolet radiation‐induced tumor development by modulation of immune and inflammatory responses

2020 ◽  
Vol 60 (1) ◽  
pp. 60-70
Author(s):  
Israr Ahmad ◽  
Tahseen H. Nasti ◽  
Heba M. Rihan ◽  
Hugo Jimenez ◽  
Craig A. Elmets ◽  
...  
Keyword(s):  
Ultraviolet Radiation ◽  
Inflammatory Responses ◽  
Tumor Development ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

Abstract 525: Toll-like receptor-4 mediated cutaneous immune responses augment ultraviolet radiation-induced DNA damage and tumor development

2012 ◽  
Author(s):  
Israr Ahmad ◽  
Purushotham Guroji ◽  
Hugo Jimenez ◽  
Eva Simanyi ◽  
Anusuiya Nagar ◽  
...  
Keyword(s):  
Dna Damage ◽  
Immune Responses ◽  
Ultraviolet Radiation ◽  
Tumor Development ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

scholarly journals 513 The toll like receptor-4 antagonist, TAK-242, enhances repair of ultraviolet radiation-induced DNA damage and inhibits UVB-induced tumor development in mice

2021 ◽  
Vol 141 (5) ◽  
pp. S89
Author(s):  
M.A. Sherwani ◽  
A.S. Abdelgawad ◽  
M. Eraslan ◽  
M. Chung ◽  
C. Elmets ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ultraviolet Radiation ◽  
Tumor Development ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

scholarly journals Regulation of ultraviolet radiation induced cutaneous photoimmunosuppression by Toll-like receptor-4

2011 ◽  
Vol 508 (2) ◽  
pp. 171-177 ◽  
Author(s):  
Wesley Lewis ◽  
Eva Simanyi ◽  
Hui Li ◽  
Camilla A. Thompson ◽  
Tahseen H. Nasti ◽  
...  
Keyword(s):  
Ultraviolet Radiation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

scholarly journals Biofilm Growth Increases Phosphorylcholine Content and Decreases Potency of Nontypeable Haemophilus influenzae Endotoxins

2006 ◽  
Vol 74 (3) ◽  
pp. 1828-1836 ◽  
Author(s):  
Shayla West-Barnette ◽  
Andrea Rockel ◽  
W. Edward Swords
Keyword(s):  
Haemophilus Influenzae ◽  
Inflammatory Responses ◽  
Opportunistic Pathogen ◽  
Host Responses ◽  
Toll Like Receptor ◽  
Nontypeable Haemophilus Influenzae ◽  
Toll Like Receptor 4 ◽  
Biofilm Growth ◽  
Bacterial Endotoxins ◽  
Cell Layers

ABSTRACT Nontypeable Haemophilus influenzae (NTHI) is a common respiratory commensal and opportunistic pathogen. NTHI is normally contained within the airways by host innate defenses that include recognition of bacterial endotoxins by Toll-like receptor 4 (TLR4). NTHI produces lipooligosaccharide (LOS) endotoxins which lack polymeric O side chains and which may contain host glycolipids. We recently showed that NTHI biofilms contain variants with sialylated LOS glycoforms that are essential to biofilm formation. In this study, we show that NTHI forms biofilms on epithelial cell layers. Confocal analysis revealed that sialylated variants were distributed throughout the biofilm, while variants expressing phosphorylcholine (PCho) were found within the biofilm. Consistent with this observation, PCho content of LOS purified from NTHI biofilms was increased compared to LOS from planktonic cultures. Hypothesizing that the observed changes in endotoxin composition could affect bioactivity, we compared inflammatory responses to NTHI LOS purified from biofilm and planktonic cultures. Our results show that endotoxins from biofilms induced weaker host innate responses. While we observed a minimal effect of sialylation on LOS bioactivity, there was a significant decrease in bioactivity associated with PCho substitutions. We thus conclude that biofilm growth increases the proportion of PCho+ variants in an NTHI population, resulting in a net decrease in LOS bioactivity. Thus, in addition to their well-documented resistance phenotypes, our data show that biofilm communities of NTHI bacteria contain variants that evoke less potent host responses.

scholarly journals Interleukin-17 Mediated Inflammatory Responses Are Required for Ultraviolet Radiation-Induced Immune Suppression

2014 ◽  
Vol 91 (1) ◽  
pp. 235-241 ◽  
Author(s):  
Hui Li ◽  
Ram Prasad ◽  
Santosh K. Katiyar ◽  
Nabiha Yusuf ◽  
Craig A. Elmets ◽  
...  
Keyword(s):  
Ultraviolet Radiation ◽  
Immune Suppression ◽  
Inflammatory Responses ◽  
Interleukin 17 ◽  
Radiation Induced

scholarly journals Human resistin protects against endotoxic shock by blocking LPS–TLR4 interaction

2017 ◽  
Vol 114 (48) ◽  
pp. E10399-E10408 ◽  
Author(s):  
Jessica C. Jang ◽  
Jiang Li ◽  
Luca Gambini ◽  
Hashini M. Batugedara ◽  
Sandeep Sati ◽  
...  
Keyword(s):  
Immune Cell ◽  
Inflammatory Responses ◽  
Endotoxic Shock ◽  
Critical Role ◽  
Nippostrongylus Brasiliensis ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Therapeutic Function ◽  
Human Immune ◽  
Human Resistin

Helminths trigger multiple immunomodulatory pathways that can protect from sepsis. Human resistin (hRetn) is an immune cell-derived protein that is highly elevated in helminth infection and sepsis. However, the function of hRetn in sepsis, or whether hRetn influences helminth protection against sepsis, is unknown. Employing hRetn-expressing transgenic mice (hRETNTg+) and recombinant hRetn, we identify a therapeutic function for hRetn in lipopolysaccharide (LPS)-induced septic shock. hRetn promoted helminth-induced immunomodulation, with increased survival of Nippostrongylus brasiliensis (Nb)-infected hRETNTg+ mice after a fatal LPS dose compared with naive mice or Nb-infected hRETNTg− mice. Employing immunoprecipitation assays, hRETNTg+Tlr4−/− mice, and human immune cell culture, we demonstrate that hRetn binds the LPS receptor Toll-like receptor 4 (TLR4) through its N terminal and modulates STAT3 and TBK1 signaling, triggering a switch from proinflammatory to anti-inflammatory responses. Further, we generate hRetn N-terminal peptides that are able to block LPS proinflammatory function. Together, our studies identify a critical role for hRetn in blocking LPS function with important clinical significance in helminth-induced immunomodulation and sepsis.

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