scholarly journals Tissue-Specific Patterning of Host Innate Immune Responses by Staphylococcus aureus α-Toxin

2014 ◽  
Vol 6 (5) ◽  
pp. 619-631 ◽  
Author(s):  
Russell E.N. Becker ◽  
Bryan J. Berube ◽  
Georgia R. Sampedro ◽  
Andrea C. DeDent ◽  
Juliane Bubeck Wardenburg
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Tissue Specific

scholarly journals A mouse ear skin model to study the dynamics of innate immune responses against Staphylococcus aureus biofilms

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Aizat Iman Abdul Hamid ◽  
Laurence Nakusi ◽  
Mickael Givskov ◽  
Young-Tae Chang ◽  
Claire Marquès ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Skin Model ◽  
Mouse Ear

Tissue-specific Regulation of Innate Immune Responses by Human Cathelicidin LL-37

2018 ◽  
Vol 24 (10) ◽  
pp. 1079-1091 ◽  
Author(s):  
Panjit Chieosilapatham ◽  
Shigaku Ikeda ◽  
Hideoki Ogawa ◽  
Francois Niyonsaba
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Anatomical Distribution ◽  
Tissue Specific ◽  
Proliferation And Differentiation ◽  
Host Origin ◽  
Specific Factors ◽  
Specific Regulation

Cathelicidins form one of the major families of antimicrobial peptides and have been identified in many vertebrates, including humans. LL-37, the only human member of the cathelicidin family, is detected in most sites of the human body that is normally exposed to microbes, including the epithelial lining of the skin, gastrointestinal tract, genitourinary tract and lungs. This peptide is also expressed by a variety of epithelial cells and immune cells, such as neutrophils, monocytes and mast cells. LL-37 has emerged as a key component of innate immunity due to its direct antimicrobial activity against a broad spectrum of invading pathogens. It also exhibits diverse immunomodulatory functions by activating both pro- and anti-inflammatory mediators; inducing cell migration, proliferation and differentiation; and regulating apoptosis of epithelial cells and neutrophils. Given that the phenotypic and functional properties of immune compartments are different and significantly impacted by the anatomical sites, tissue-specific factors of host origin and microbial communities play important roles in the regulation of LL-37. This review summarizes the expression and biological functions of LL-37 and discusses its significant roles in the innate immune system based on its anatomical distribution.

scholarly journals Escherichia coli and Staphylococcus aureus Elicit Differential Innate Immune Responses following Intramammary Infection

2004 ◽  
Vol 11 (3) ◽  
pp. 463-472 ◽  
Author(s):  
Douglas D. Bannerman ◽  
Max J. Paape ◽  
Jai-Wei Lee ◽  
Xin Zhao ◽  
Jayne C. Hope ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Clinical Mastitis ◽  
Cytokine Response ◽  
Innate Immune ◽  
Host Recognition ◽  
Innate Immune Responses ◽  
E Coli ◽  
Intramammary Infection

ABSTRACTStaphylococcus aureusandEscherichia coliare among the most prevalent species of gram-positive and gram-negative bacteria, respectively, that induce clinical mastitis. The innate immune system comprises the immediate host defense mechanisms to protect against infection and contributes to the initial detection of and proinflammatory response to infectious pathogens. The objective of the present study was to characterize the different innate immune responses to experimental intramammary infection withE. coliandS. aureusduring clinical mastitis. The cytokine response and changes in the levels of soluble CD14 (sCD14) and lipopolysaccharide-binding protein (LBP), two proteins that contribute to host recognition of bacterial cell wall products, were studied. Intramammary infection with eitherE. coliorS. aureuselicited systemic changes, including decreased milk output, a febrile response, and induction of the acute-phase synthesis of LBP. Infection with either bacterium resulted in increased levels of interleukin 1β (IL-1β), gamma interferon, IL-12, sCD14, and LBP in milk. High levels of the complement cleavage product C5a and the anti-inflammatory cytokine IL-10 were detected at several time points followingE. coliinfection, whereasS. aureusinfection elicited a slight but detectable increase in these mediators at a single time point. Increases in IL-8 and tumor necrosis factor alpha were observed only in quarters infected withE. coli. Together, these data demonstrate the variability of the host innate immune response toE. coliandS. aureusand suggest that the limited cytokine response toS. aureusmay contribute to the well-known ability of the bacterium to establish chronic intramammary infection.

scholarly journals The Resistance to Host Antimicrobial Peptides in Infections Caused by Daptomycin-Resistant Staphylococcus aureus

Antibiotics ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 96
Author(s):  
Md Saruar Bhuiyan ◽  
Jhih-Hang Jiang ◽  
Xenia Kostoulias ◽  
Ravali Theegala ◽  
Graham J. Lieschke ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Antimicrobial Peptides ◽  
Innate Immune ◽  
Cross Resistance ◽  
Infection Model ◽  
Innate Immune Responses ◽  
Persistent Infections ◽  
Zebrafish Infection

Daptomycin is an important antibiotic for the treatment of infections caused by Staphylococcus aureus. The emergence of daptomycin resistance in S. aureus is associated with treatment failure and persistent infections with poor clinical outcomes. Here, we investigated host innate immune responses against clinically derived, daptomycin-resistant (DAP-R) and -susceptible S. aureus paired isolates using a zebrafish infection model. We showed that the control of DAP-R S. aureus infections was attenuated in vivo due to cross-resistance to host cationic antimicrobial peptides. These data provide mechanistic understanding into persistent infections caused by DAP-R S. aureus and provide crucial insights into the adaptive evolution of this troublesome pathogen.

Sign in / Sign up

Export Citation Format

Share Document