anbuo92

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?:abstract	BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly reached pandemic proportions. Given that the main target of SARS-CoV-2 are lungs leading to severe pneumonia with hyperactivation of the inflammatory cascade, we conducted a prospective study to assess alveolar inflammatory status in patients with moderate to severe COVID-19. METHODS: Diagnostic bronchoalveolar lavage (BAL) was performed in 33 adult patients with SARS-CoV-2 infection by real-time PCR on nasopharyngeal swab admitted to the Intensive care unit (ICU) (n = 28) and to the Intermediate Medicine Ward (IMW) (n = 5). We analyze the differential cell count, ultrastructure of cells and Interleukin (IL)6, 8 and 10 levels. RESULTS: ICU patients showed a marked increase in neutrophils (1.24 × 10(5) ml(− 1), 0.85–2.07), lower lymphocyte (0.97 × 10(5) ml(− 1), 0.024–0.34) and macrophages fractions (0.43 × 10(5) ml(− 1), 0.34–1.62) compared to IMW patients (0.095 × 10(5) ml(− 1), 0.05–0.73; 0.47 × 10(5) ml(− 1), 0.28–1.01 and 2.14 × 10(5) ml(− 1), 1.17–3.01, respectively) (p < 0.01). Study of ICU patients BAL by electron transmission microscopy showed viral particles inside mononuclear cells confirmed by immunostaining with anti-viral capsid and spike antibodies. IL6 and IL8 were significantly higher in ICU patients than in IMW (IL6 p < 0.01, IL8 p < 0.0001), and also in patients who did not survive (IL6 p < 0.05, IL8 p = 0.05 vs. survivors). IL10 did not show a significant variation between groups. Dividing patients by treatment received, lower BAL concentrations of IL6 were found in patients treated with steroids as compared to those treated with tocilizumab (p < 0.1) or antivirals (p < 0.05). CONCLUSIONS: Alveolitis, associated with COVID-19, is mainly sustained by innate effectors which showed features of extensive activation. The burden of pro-inflammatory cytokines IL6 and IL8 in the broncho-alveolar environment is associated with clinical outcome. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12890-020-01343-z.
is ?:annotates of	<https://research.tib.eu/covid-19/entity/6anbuo92_hasAnnotation_C0003451> <https://research.tib.eu/covid-19/entity/6anbuo92_hasAnnotation_C0013227> <https://research.tib.eu/covid-19/entity/6anbuo92_hasAnnotation_C0021368> <https://research.tib.eu/covid-19/entity/6anbuo92_hasAnnotation_C5203676>
?:creator	<https://research.tib.eu/covid-19/entity/Pandolfi%2C_Laura%3B_Fossali%2C_Tommaso%3B_Frangipane%2C_Vanessa%3B_Bozzini%2C_Sara%3B_Morosini%2C_Monica%3B_D%E2%80%99Amato%2C_Maura%3B_Lettieri%2C_Sara%3B_Urtis%2C_Mario%3B_Di_Toro%2C_Alessandro%3B_Saracino%2C_Laura%3B_Percivalle%2C_Elena%3B_Tomaselli%2C_Stefano%3B_Cavagna%2C_Lorenzo%3B_Cova%2C_Emanuela%3B_Mojoli%2C_Francesco%3B_Bergomi%2C_Paola%3B_Ottolina%2C_Davide%3B_Lilleri%2C_Daniele%3B_Corsico%2C_Angelo_Guido%3B_Arbustini%2C_Eloisa%3B_Colombo%2C_Riccardo%3B_Meloni%2C_Federica>
?:doi	10.1186/s12890-020-01343-z
?:doi	<https://research.tib.eu/covid-19/entity/10.1186/s12890-020-01343-z>
?:journal	BMC_Pulm_Med
?:license	cc-by
?:pdf_json_files	document_parses/pdf_json/622688632938200ed27972924e2a19ed0c5ee932.json
?:pmc_json_files	document_parses/pmc_json/PMC7668012.xml.json
?:pmcid	<https://research.tib.eu/covid-19/entity/PMC7668012>
?:pmid	<https://research.tib.eu/covid-19/entity/33198751.0>
?:pmid	33198751.0
?:publication_isRelatedTo_Disease	<https://research.tib.eu/covid-19/entity/COVID-19>
is ?:relation_isRelatedTo_publication of	<https://research.tib.eu/covid-19/entity/6anbuo92_HAS_C5203670_COEXISTS_WITH_C0549493> <https://research.tib.eu/covid-19/entity/6anbuo92_HAS_C5203676_CAUSES_C0032285>
?:sha_id	<https://research.tib.eu/covid-19/entity/622688632938200ed27972924e2a19ed0c5ee932>
?:source	Medline; PMC
?:title	Broncho-alveolar inflammation in COVID-19 patients: a correlation with clinical outcome
?:type	<https://research.tib.eu/covid-19/vocab/Publication>
?:year	2020-11-16

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Value

?:abstract

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly reached pandemic proportions. Given that the main target of SARS-CoV-2 are lungs leading to severe pneumonia with hyperactivation of the inflammatory cascade, we conducted a prospective study to assess alveolar inflammatory status in patients with moderate to severe COVID-19. METHODS: Diagnostic bronchoalveolar lavage (BAL) was performed in 33 adult patients with SARS-CoV-2 infection by real-time PCR on nasopharyngeal swab admitted to the Intensive care unit (ICU) (n = 28) and to the Intermediate Medicine Ward (IMW) (n = 5). We analyze the differential cell count, ultrastructure of cells and Interleukin (IL)6, 8 and 10 levels. RESULTS: ICU patients showed a marked increase in neutrophils (1.24 × 10(5) ml(− 1), 0.85–2.07), lower lymphocyte (0.97 × 10(5) ml(− 1), 0.024–0.34) and macrophages fractions (0.43 × 10(5) ml(− 1), 0.34–1.62) compared to IMW patients (0.095 × 10(5) ml(− 1), 0.05–0.73; 0.47 × 10(5) ml(− 1), 0.28–1.01 and 2.14 × 10(5) ml(− 1), 1.17–3.01, respectively) (p < 0.01). Study of ICU patients BAL by electron transmission microscopy showed viral particles inside mononuclear cells confirmed by immunostaining with anti-viral capsid and spike antibodies. IL6 and IL8 were significantly higher in ICU patients than in IMW (IL6 p < 0.01, IL8 p < 0.0001), and also in patients who did not survive (IL6 p < 0.05, IL8 p = 0.05 vs. survivors). IL10 did not show a significant variation between groups. Dividing patients by treatment received, lower BAL concentrations of IL6 were found in patients treated with steroids as compared to those treated with tocilizumab (p < 0.1) or antivirals (p < 0.05). CONCLUSIONS: Alveolitis, associated with COVID-19, is mainly sustained by innate effectors which showed features of extensive activation. The burden of pro-inflammatory cytokines IL6 and IL8 in the broncho-alveolar environment is associated with clinical outcome. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12890-020-01343-z.

is ?:annotates of