scholarly journals Diverse Functions of Pulmonary Collectins in Host Defense of the Lung

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Shigeru Ariki ◽  
Chiaki Nishitani ◽  
Yoshio Kuroki

Pulmonary surfactant is a mixture of lipids and proteins that covers alveolar surfaces and keeps alveoli from collapsing. Four specific proteins have been identified in surfactant. Among them, two C-type lectins, surfactant proteins A and D (SP-A and SP-D), are known to be implicated in host defense and regulation of inflammatory responses of the lung. These host defense lectins are structurally characterized by N-terminal collagen-like domains and lectin domains and are called pulmonary collectins. They prevent dissemination of infectious microbes by their biological activities including agglutination and growth inhibition. They also promote clearance of microbes by enhancing phagocytosis in macrophages. In addition, they interact with the other pattern-recognition molecules, including Toll-like receptors (TLRs) and TLR-associated molecules, CD14 and MD-2, and regulate inflammatory responses. Furthermore, recent studies have demonstrated that these collectins modulate functions of neutrophil-derived innate immune molecules by interacting with them. These findings indicate that pulmonary collectins play critical roles in host defense of the lung.

Author(s):  
Guobin Chang ◽  
Lingling Qiu ◽  
Xiangping Liu ◽  
Zhiteng Li ◽  
Wei Lu ◽  
...  

As we all known, NLRC5 recognizes intracellular pathogen-associated molecular patterns (PAMPs) and provokes innate immune system. Its role in innate immune response, NF-kB activation and MHC-I expression remains controversial. In the present study, it was detected that differential gene expressions in NLRC5 signaling pathway at 2, 4, 6 and 8 hours after exposure to LPS using qRT-PCR technology, then analyzed its roles in host defense. The results showed that, comparing to control groups, the expression of NLRC5, MHC-I and IL-18 in LPS-treated groups were significantly up-regulated at 2 hours post stimulation (hps), TLR4 and NF-kB showed conspicuously up-regulated at 4 hps, while STAT1 was significantly down-regulated at 8 hps. Collectively, LPS did evoke inflammatory responses and NLRC5 may negatively regulate NF-kB and critically regulate MHC-I to control intracellular PAMPs in chicken macrophage cell line but the specific role of NLRC5 in host defense relates to cell types and species tested.


2004 ◽  
Vol 279 (31) ◽  
pp. 32728-32736 ◽  
Author(s):  
Nades Palaniyar ◽  
Jeya Nadesalingam ◽  
Howard Clark ◽  
Michael J. Shih ◽  
Alister W. Dodds ◽  
...  

2006 ◽  
Vol 85 (6) ◽  
pp. 524-529 ◽  
Author(s):  
Y. Sugawara ◽  
A. Uehara ◽  
Y. Fujimoto ◽  
S. Kusumoto ◽  
K. Fukase ◽  
...  

Oral epithelium might be the first barrier against oral bacteria in periodontal tissue. We hypothesized that oral epithelium is endowed with innate immune receptors for bacterial components, which play roles in host defense against bacterial infection without being accompanied by excessive inflammatory responses. We found clear expression of Toll-like receptor (TLR)4 as well as TLR2, and strong expression of NOD1 and NOD2 in normal oral epithelial tissues by immunohistochemical analysis. We also showed that primary oral epithelial cells in culture expressed these molecules using PCR, flow cytometry, and immunostaining. In inflamed oral epithelium, cell-surface localizations of TLR2 and TLR4 were more clearly observed than in healthy tissue. Upon stimulation with synthetic ligands for these receptors, the expression of β-defensin 2 was markedly up-regulated. These findings indicate that these molecules in oral epithelial cells are functional receptors that induce antibacterial responses.


ExRNA ◽  
2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Ava Behrouzi ◽  
Marjan Alimohammadi ◽  
Amir Hossein Nafari ◽  
Mohammad Hadi Yousefi ◽  
Farhad Riazi Rad ◽  
...  

Abstract MicroRNAs are non-coding RNAs, playing an important role in regulating many biological pathways, such as innate immune response against various infections. Different studies confirm that many miRNAs act as important regulators in developing a strategy for the survival of Mycobacterium tuberculosis in the host cell. On the other hand, an innate immune response is one of the important aspects of host defense against Mycobacterium. Considering the importance of miRNAs during tuberculosis infection, we focused on studies that performed on the role of various miRNAs related to pathogenic bacteria, M. tuberculosis in the host. Also, we have introduced important miRNAs that can be used as a biomarker for the detection of Mycobacterium.


Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1175
Author(s):  
Chiara Geyer ◽  
Lynn Mes ◽  
Melissa Newling ◽  
Jeroen den Dunnen ◽  
Willianne Hoepel

Macrophages play a key role in induction of inflammatory responses. These inflammatory responses are mostly considered to be instigated by activation of pattern recognition receptors (PRRs) or cytokine receptors. However, recently it has become clear that also antibodies and pentraxins, which can both activate Fc receptors (FcRs), induce very powerful inflammatory responses by macrophages that can even be an order of magnitude greater than PRRs. While the physiological function of this antibody-dependent inflammation (ADI) is to counteract infections, undesired activation or over-activation of this mechanism will lead to pathology, as observed in a variety of disorders, including viral infections such as COVID-19, chronic inflammatory disorders such as Crohn’s disease, and autoimmune diseases such as rheumatoid arthritis. In this review we discuss how physiological ADI provides host defense by inducing pathogen-specific immunity, and how erroneous activation of this mechanism leads to pathology. Moreover, we will provide an overview of the currently known signaling and metabolic pathways that underlie ADI, and how these can be targeted to counteract pathological inflammation.


2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
Kathleen L. McCoy

Since the discovery of the endocannabinoid system consisting of cannabinoid receptors, endogenous ligands, and biosynthetic and metabolizing enzymes, interest has been renewed in investigating the promise of cannabinoids as therapeutic agents. Abundant evidence indicates that cannabinoids modulate immune responses. An inflammatory response is triggered when innate immune cells receive a danger signal provided by pathogen- or damage-associated molecular patterns engaging pattern-recognition receptors. Toll-like receptor family members are prominent pattern-recognition receptors expressed on innate immune cells. Cannabinoids suppress Toll-like receptor-mediated inflammatory responses. However, the relationship between the endocannabinoid system and innate immune system may not be one-sided. Innate immune cells express cannabinoid receptors and produce endogenous cannabinoids. Hence, innate immune cells may play a role in regulating endocannabinoid homeostasis, and, in turn, the endocannabinoid system modulates local inflammatory responses. Studies designed to probe the interaction between the innate immune system and the endocannabinoid system may identify new potential molecular targets in developing therapeutic strategies for chronic inflammatory diseases. This review discusses the endocannabinoid system and Toll-like receptor family and evaluates the interaction between them.


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