Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis

Coagulase-negative staphylococci (CoNS), including Staphylococcus (S) epidermidis, are responsible for ~70% of all post-surgical endophthalmitis, a potentially blinding eye infection. However, the pathobiology of CoNS endophthalmitis is limited to epidemiological and clinical case studies with few e...

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Autores principales:	Susmita Das, Sukhvinder Singh, Ashok Kumar
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	eye retina endophthalmitis Staphylococcus epidermidis innate immunity inflammation Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/90984bfcc07d43b7b56df2c7d99d475a
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spelling	oai:doaj.org-article:90984bfcc07d43b7b56df2c7d99d475a2021-11-17T07:02:11ZBacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis2235-298810.3389/fcimb.2021.780648https://doaj.org/article/90984bfcc07d43b7b56df2c7d99d475a2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcimb.2021.780648/fullhttps://doaj.org/toc/2235-2988Coagulase-negative staphylococci (CoNS), including Staphylococcus (S) epidermidis, are responsible for ~70% of all post-surgical endophthalmitis, a potentially blinding eye infection. However, the pathobiology of CoNS endophthalmitis is limited to epidemiological and clinical case studies with few experimental studies. Here, we report both in vitro and in vivo models to study the pathobiology of S. epidermidis endophthalmitis in mice. We found that S. epidermidis is rapidly cleared from mouse eyes, and a relatively higher dose (i.e., 107 CFU/eye) was needed to cause endophthalmitis. Our time-course study revealed that bacterial load peaked at 24 h post-infection followed by a gradual decline up to 72 h. A similar time-dependent decrease in levels of inflammatory mediators and Toll-like receptor (TLR) expression was also observed. In contrast, neutrophil infiltration continued to increase up to 72 h coinciding with significant retinal tissue damage and loss of visual function. In vitro, S. epidermidis induced the activation of various inflammatory signaling pathways (i.e., NF-kB, ERK, and P38) and the production of both cytokines and chemokines in mouse BMDMs, human RPE, and retinal Muller glia. Altogether, we show that bacterial burden is reduced in S. epidermidis endophthalmitis, while tissue damage and visual function loss continue. Thus, our study provides new insights into the pathogenesis of CoNS endophthalmitis.Susmita DasSukhvinder SinghAshok KumarAshok KumarFrontiers Media S.A.articleeyeretinaendophthalmitisStaphylococcus epidermidisinnate immunityinflammationMicrobiologyQR1-502ENFrontiers in Cellular and Infection Microbiology, Vol 11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	eye retina endophthalmitis Staphylococcus epidermidis innate immunity inflammation Microbiology QR1-502
spellingShingle	eye retina endophthalmitis Staphylococcus epidermidis innate immunity inflammation Microbiology QR1-502 Susmita Das Sukhvinder Singh Ashok Kumar Ashok Kumar Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis
description	Coagulase-negative staphylococci (CoNS), including Staphylococcus (S) epidermidis, are responsible for ~70% of all post-surgical endophthalmitis, a potentially blinding eye infection. However, the pathobiology of CoNS endophthalmitis is limited to epidemiological and clinical case studies with few experimental studies. Here, we report both in vitro and in vivo models to study the pathobiology of S. epidermidis endophthalmitis in mice. We found that S. epidermidis is rapidly cleared from mouse eyes, and a relatively higher dose (i.e., 107 CFU/eye) was needed to cause endophthalmitis. Our time-course study revealed that bacterial load peaked at 24 h post-infection followed by a gradual decline up to 72 h. A similar time-dependent decrease in levels of inflammatory mediators and Toll-like receptor (TLR) expression was also observed. In contrast, neutrophil infiltration continued to increase up to 72 h coinciding with significant retinal tissue damage and loss of visual function. In vitro, S. epidermidis induced the activation of various inflammatory signaling pathways (i.e., NF-kB, ERK, and P38) and the production of both cytokines and chemokines in mouse BMDMs, human RPE, and retinal Muller glia. Altogether, we show that bacterial burden is reduced in S. epidermidis endophthalmitis, while tissue damage and visual function loss continue. Thus, our study provides new insights into the pathogenesis of CoNS endophthalmitis.
format	article
author	Susmita Das Sukhvinder Singh Ashok Kumar Ashok Kumar
author_facet	Susmita Das Sukhvinder Singh Ashok Kumar Ashok Kumar
author_sort	Susmita Das
title	Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis
title_short	Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis
title_full	Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis
title_fullStr	Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis
title_full_unstemmed	Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis
title_sort	bacterial burden declines but neutrophil infiltration and ocular tissue damage persist in experimental staphylococcus epidermidis endophthalmitis
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/90984bfcc07d43b7b56df2c7d99d475a
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Bacterial Burden Declines But Neutrophil Infiltration and Ocular Tissue Damage Persist in Experimental Staphylococcus epidermidis Endophthalmitis

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