qryzx9mb

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?:abstract	BACKGROUND AND AIMS: Gastrointestinal (GI) manifestations have been increasingly reported in Coronavirus Disease 2019 (COVID-19) patients However, the roles of the GI tract in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection are not fully understood We investigated how the GI tract is involved in SARS-CoV-2 infection to elucidate the pathogenesis of COVID-19 METHODS: Our previously established nonhuman primate (NHP) model of COVID-19 was modified in this study to test our hypothesis Rhesus monkeys were infected with an intragastric or intranasal challenge with SARS-CoV-2 Clinical signs were recorded after infection Viral genomic RNA was quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) Host responses to SARS-CoV-2 infection were evaluated by examining inflammatory cytokines, macrophages, histopathology and mucin barrier integrity RESULTS: Intranasal inoculation with SARS-CoV-2 led to infections and pathological changes not only in respiratory tissues but also in digestive tissues Expectedly, intragastric inoculation with SARS-CoV-2 resulted in the productive infection of digestive tissues and inflammation in both the lung and digestive tissues Inflammatory cytokines were induced by both types of inoculation with SARS-CoV-2, consistent with the increased expression of CD68 Immunohistochemistry and alcian blue/periodic acid-Schiff (AB-PAS) staining showed decreased Ki67, increased cleaved caspase 3 and decreased numbers of mucin-containing goblet cells, suggesting that the inflammation induced by these two types of inoculation with SARS-CoV-2 impaired the GI barrier and caused severe infections CONCLUSIONS: Both intranasal and intragastric inoculation with SARS-CoV-2 caused pneumonia and GI dysfunction in our rhesus monkey model Inflammatory cytokines are possible connections for the pathogenesis of SARS-CoV-2 between the respiratory and digestive systems BACKGROUND AND AIMS: Gastrointestinal (GI) manifestations have been increasingly reported in Coronavirus Disease 2019 (COVID-19) patients. However, the roles of the GI tract in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection are not fully understood. We investigated how the GI tract is involved in SARS-CoV-2 infection to elucidate the pathogenesis of COVID-19. METHODS: Our previously established nonhuman primate (NHP) model of COVID-19 was modified in this study to test our hypothesis. Rhesus monkeys were infected with an intragastric or intranasal challenge with SARS-CoV-2. Clinical signs were recorded after infection. Viral genomic RNA was quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Host responses to SARS-CoV-2 infection were evaluated by examining inflammatory cytokines, macrophages, histopathology and mucin barrier integrity. RESULTS: Intranasal inoculation with SARS-CoV-2 led to infections and pathological changes not only in respiratory tissues but also in digestive tissues. Expectedly, intragastric inoculation with SARS-CoV-2 resulted in the productive infection of digestive tissues and inflammation in both the lung and digestive tissues. Inflammatory cytokines were induced by both types of inoculation with SARS-CoV-2, consistent with the increased expression of CD68. Immunohistochemistry and alcian blue/periodic acid-Schiff (AB-PAS) staining showed decreased Ki67, increased cleaved caspase 3 and decreased numbers of mucin-containing goblet cells, suggesting that the inflammation induced by these two types of inoculation with SARS-CoV-2 impaired the GI barrier and caused severe infections. CONCLUSIONS: Both intranasal and intragastric inoculation with SARS-CoV-2 caused pneumonia and GI dysfunction in our rhesus monkey model. Inflammatory cytokines are possible connections for the pathogenesis of SARS-CoV-2 between the respiratory and digestive systems.
is ?:annotates of	<https://research.tib.eu/covid-19/entity/qryzx9mb_hasAnnotation_C0017428> <https://research.tib.eu/covid-19/entity/qryzx9mb_hasAnnotation_C0021368> <https://research.tib.eu/covid-19/entity/qryzx9mb_hasAnnotation_C0035736> <https://research.tib.eu/covid-19/entity/qryzx9mb_hasAnnotation_C1334508> <https://research.tib.eu/covid-19/entity/qryzx9mb_hasAnnotation_C3714514> <https://research.tib.eu/covid-19/entity/qryzx9mb_hasAnnotation_C5203676>
?:creator	<https://research.tib.eu/covid-19/entity/Jiao%2C_L.%3B_Li%2C_H.%3B_Xu%2C_J.%3B_Yang%2C_M.%3B_Ma%2C_C.%3B_Li%2C_J.%3B_Zhao%2C_S.%3B_Wang%2C_H.%3B_Yang%2C_Y.%3B_Yu%2C_W.%3B_Wang%2C_J.%3B_Yang%2C_J.%3B_Long%2C_H.%3B_Gao%2C_J.%3B_Ding%2C_K.%3B_Wu%2C_D.%3B_Kuang%2C_D.%3B_Zhao%2C_Y.%3B_Liu%2C_J.%3B_Lu%2C_S.%3B_Liu%2C_H.%3B_Peng%2C_X.> <https://research.tib.eu/covid-19/entity/Jiao%2C_Li%3B_Li%2C_Haiyan%3B_Xu%2C_Jingwen%3B_Yang%2C_Mengli%3B_Ma%2C_Chunxia%3B_Li%2C_Jingmei%3B_Zhao%2C_Siwen%3B_Wang%2C_Haixuan%3B_Yang%2C_Yun%3B_Yu%2C_Wenhai%3B_Wang%2C_Junbin%3B_Yang%2C_Jing%3B_Long%2C_Haiting%3B_Gao%2C_Jiahong%3B_Ding%2C_Kaiyun%3B_Wu%2C_Daoju%3B_Kuang%2C_Dexuan%3B_Zhao%2C_Yuan%3B_Liu%2C_Jiansheng%3B_Lu%2C_Shuaiyao%3B_Liu%2C_Hongqi%3B_Peng%2C_Xiaozhong>
?:journal	Gastroenterology
?:license	unk
?:publication_isRelatedTo_Disease	<https://research.tib.eu/covid-19/entity/COVID-19>
is ?:relation_isRelatedTo_publication of	<https://research.tib.eu/covid-19/entity/qryzx9mb_HAS_C1334508_STIMULATES_C0291573> <https://research.tib.eu/covid-19/entity/qryzx9mb_HAS_C2949227_INHIBITS_C1334508> <https://research.tib.eu/covid-19/entity/qryzx9mb_HAS_C5203676_CAUSES_C3714514>
?:source	WHO
?:title	The gastrointestinal tract is an alternative route for SARS-CoV-2 infection in a nonhuman primate model
?:type	<https://research.tib.eu/covid-19/vocab/Publication>
?:who_covidence_id	#1065985 #967289
?:year	2020

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?:abstract

BACKGROUND AND AIMS: Gastrointestinal (GI) manifestations have been increasingly reported in Coronavirus Disease 2019 (COVID-19) patients However, the roles of the GI tract in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection are not fully understood We investigated how the GI tract is involved in SARS-CoV-2 infection to elucidate the pathogenesis of COVID-19 METHODS: Our previously established nonhuman primate (NHP) model of COVID-19 was modified in this study to test our hypothesis Rhesus monkeys were infected with an intragastric or intranasal challenge with SARS-CoV-2 Clinical signs were recorded after infection Viral genomic RNA was quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) Host responses to SARS-CoV-2 infection were evaluated by examining inflammatory cytokines, macrophages, histopathology and mucin barrier integrity RESULTS: Intranasal inoculation with SARS-CoV-2 led to infections and pathological changes not only in respiratory tissues but also in digestive tissues Expectedly, intragastric inoculation with SARS-CoV-2 resulted in the productive infection of digestive tissues and inflammation in both the lung and digestive tissues Inflammatory cytokines were induced by both types of inoculation with SARS-CoV-2, consistent with the increased expression of CD68 Immunohistochemistry and alcian blue/periodic acid-Schiff (AB-PAS) staining showed decreased Ki67, increased cleaved caspase 3 and decreased numbers of mucin-containing goblet cells, suggesting that the inflammation induced by these two types of inoculation with SARS-CoV-2 impaired the GI barrier and caused severe infections CONCLUSIONS: Both intranasal and intragastric inoculation with SARS-CoV-2 caused pneumonia and GI dysfunction in our rhesus monkey model Inflammatory cytokines are possible connections for the pathogenesis of SARS-CoV-2 between the respiratory and digestive systems
BACKGROUND AND AIMS: Gastrointestinal (GI) manifestations have been increasingly reported in Coronavirus Disease 2019 (COVID-19) patients. However, the roles of the GI tract in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection are not fully understood. We investigated how the GI tract is involved in SARS-CoV-2 infection to elucidate the pathogenesis of COVID-19. METHODS: Our previously established nonhuman primate (NHP) model of COVID-19 was modified in this study to test our hypothesis. Rhesus monkeys were infected with an intragastric or intranasal challenge with SARS-CoV-2. Clinical signs were recorded after infection. Viral genomic RNA was quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Host responses to SARS-CoV-2 infection were evaluated by examining inflammatory cytokines, macrophages, histopathology and mucin barrier integrity. RESULTS: Intranasal inoculation with SARS-CoV-2 led to infections and pathological changes not only in respiratory tissues but also in digestive tissues. Expectedly, intragastric inoculation with SARS-CoV-2 resulted in the productive infection of digestive tissues and inflammation in both the lung and digestive tissues. Inflammatory cytokines were induced by both types of inoculation with SARS-CoV-2, consistent with the increased expression of CD68. Immunohistochemistry and alcian blue/periodic acid-Schiff (AB-PAS) staining showed decreased Ki67, increased cleaved caspase 3 and decreased numbers of mucin-containing goblet cells, suggesting that the inflammation induced by these two types of inoculation with SARS-CoV-2 impaired the GI barrier and caused severe infections. CONCLUSIONS: Both intranasal and intragastric inoculation with SARS-CoV-2 caused pneumonia and GI dysfunction in our rhesus monkey model. Inflammatory cytokines are possible connections for the pathogenesis of SARS-CoV-2 between the respiratory and digestive systems.

is ?:annotates of