SLPI and inflammatory lung disease in females

McKiernan, Paul J; McElvaney, Noel G.; Greene, Catherine M.

doi:10.1042/bst0391421

Cited by 28 publications

(21 citation statements)

References 53 publications

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“…SLPI plays an important role in anti-protease defense and exhibits anti-inflammatory, anti-bacterial, and anti-viral activities in the lungs (McKiernan et al 2011; Zani et al 2011). SLPI inhibits NF-κB-mediated pro-inflammatory gene expression, which may account for its anti-inflammatory function in the lungs (Taggart et al 2005; Weldon and Taggart 2007).…”

Section: Resultsmentioning

confidence: 99%

Common and distinct mechanisms of induced pulmonary fibrosis by particulate and soluble chemical fibrogenic agents

Dong

Porter

et al. 2015

Arch Toxicol

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Pulmonary fibrosis results from the excessive deposition of collagen fibers and scarring in the lungs with or without an identifiable cause. The mechanism(s) underlying lung fibrosis development is poorly understood, and effective treatment is lacking. Here we compared mouse lung fibrosis induced by pulmonary exposure to prototypical particulate (crystalline silica) or soluble chemical (bleomycin or paraquat) fibrogenic agents to identify the underlying mechanisms. Young male C57BL/6J mice were given silica (2 mg), bleomycin (0.07 mg), or paraquat (0.02 mg) by pharyngeal aspiration. All treatments induced significant inflammatory infiltration and collagen deposition, manifesting fibrotic foci in silica-exposed lungs or diffuse fibrosis in bleomycin or paraquat-exposed lungs on day 7 post-exposure, at which time the lesions reached their peaks and represented a junction of transition from an acute response to chronic fibrosis. Lung genomewide gene expression was analyzed, and differential gene expression was confirmed by quantitative RT-PCR, immunohistochemistry, and immunoblotting for representative genes to demonstrate their induced expression and localization in fibrotic lungs. Canonical signaling pathways, gene ontology, and upstream transcription networks modified by each agent were identified. In particular, these inducers elicited marked proliferative responses; at the same time, silica preferentially activated innate immune functions and the defense against foreign bodies, whereas bleomycin and paraquat boosted responses related to cell adhesion, platelet activation, extracellular matrix remodeling, and wound healing. This study identified, for the first time, the shared and unique genes, signaling pathways, and biological functions regulated by particulate and soluble chemical fibrogenic agents during lung fibrosis, providing insights into the mechanisms underlying human lung fibrotic diseases.

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Section: Resultsmentioning

confidence: 99%

Common and distinct mechanisms of induced pulmonary fibrosis by particulate and soluble chemical fibrogenic agents

Dong

Porter

et al. 2015

Arch Toxicol

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“…This protein is secreted from a large variety of cell types, having been found in various body fluids, especially in mucosal fluids such as bronchial fluid and saliva. In addition to an antiprotease function, SLPI alternatively possesses antimicrobial, anti-inflammatory, and immunomodulatory functions [30]. Interestingly, in B cells, SLPI can effectively suppress class switch recombination for IgA production [31].…”

Section: Discussionmentioning

confidence: 99%

MyD88 Deficiency Alters Expression of Antimicrobial Factors in Mouse Salivary Glands

et al. 2014

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The surfaces of oral mucosa are protected from infections by antimicrobial proteins and natural immunoglobulins that are constantly secreted in saliva, serving as principal innate immune defense in the oral cavity. MyD88 is an important adaptor protein for signal transduction downstream of Toll-like receptors and TACI, receptors for regulation of innate immunity and B cell responses, respectively. Although MyD88-mediated signaling has a regulatory role in the intestinal mucosal immunity, its specific role in the oral cavity has remained elusive. In the present study, we assessed the influence of MyD88 deficiency on the oral innate defense, particularly the expression of antimicrobial proteins in salivary glands and production of salivary basal immunoglobulins, in mice. Microarray analysis of the whole tissues of submandibular glands revealed that the expression of several genes encoding salivary antimicrobial proteins, such as secretory leukocyte peptidase inhibitor (SLPI), S100A8, and lactotransferrin, was reduced due to MyD88 deficiency. Histologically, SLPI-expressing acinar cells were evidently decreased in the glands from MyD88 deficient mice compared to wild-type mice. Flow cytometric analysis revealed that B cell populations, including B-1 cells and IgA+ plasma cells, residing in submandibular glands were increased by MyD88 deficiency. The level of salivary anti-phosphorylcholine IgA was elevated in MyD88 deficient mice compared to wild-type mice. Thus, this study provides a detailed description of the effect of MyD88 deficiency on expression of several salivary antimicrobial factors in mice, illustrating the role for MyD88-mediated signaling in the innate immune defense in the oral cavity.

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“…It has additionally been found to exert some immunomodulatory effects apart from its inhibition of protease activity. SLPI levels are increased in allergic asthma and levels may be upregulated by estradiol [42]. SLPI expression has also been shown to increase with high levels of circulating progesterone.…”

Section: Estrogen Effects On Allergic Diseasementioning

confidence: 99%

Estrogen effects in allergy and asthma

Bonds

Midoro-Horiuti

2013

Current Opinion in Allergy &Amp; Clinical Immunology

169

115

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Purpose of review Asthma prevalence and severity are greater in women than in men, and mounting evidence suggests this is in part related to female steroid sex hormones. Of these, estrogen has been the subject of much study. This review highlights recent research exploring the effects of estrogen in allergic disease. Recent findings Estrogen receptors are found on numerous immunoregulatory cells and estrogen’s actions skew immune responses toward allergy. It may act directly to create deleterious effects in asthma, or indirectly via modulation of various pathways including secretory leukoprotease inhibitor, transient receptor potential vanilloid type 1 ion channel and nitric oxide production to exert effects on lung mechanics and inflammation. Not only do endogenous estrogens appear to play a role, but environmental estrogens have also been implicated. Environmental estrogens (xenoestrogens) including bisphenol A and phthalates enhance allergic sensitization in animal models and may enhance development of atopic disorders like asthma in humans. Summary Estrogen’s role in allergic disease remains complex. As allergic diseases continue to increase in prevalence and affect women disproportionately, gaining a fuller understanding of its effects in these disorders will be essential. Of particular importance may be effects of xenoestrogens on allergic disease.

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SLPI and inflammatory lung disease in females

Cited by 28 publications

References 53 publications

Common and distinct mechanisms of induced pulmonary fibrosis by particulate and soluble chemical fibrogenic agents

Common and distinct mechanisms of induced pulmonary fibrosis by particulate and soluble chemical fibrogenic agents

MyD88 Deficiency Alters Expression of Antimicrobial Factors in Mouse Salivary Glands

Estrogen effects in allergy and asthma

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