TY - JOUR
T1 - Protective effect of β-glucan on Poly(I:C)-induced acute lung injury/inflammation
T2 - Therapeutic implications of viral infections in the respiratory system
AU - Tirunavalli, Satya Krishna
AU - Pramatha, Shashidhar
AU - Eedara, Abhisheik Chowdary
AU - Walvekar, Komal Paresh
AU - Immanuel, Christiana
AU - Potdar, Pooja
AU - Nayak, Pawan G.
AU - Chamallamudi, Mallikarjuna Rao
AU - Sistla, Ramakrishna
AU - Chilaka, Sabarinadh
AU - Andugulapati, Sai Balaji
N1 - Funding Information:
Authors thank the Director, CSIR-IICT, Hyderabad, India, for providing the facilities and funding necessary for the conducting of this work. CSIR-IICT manuscript communication number: IICT/Pubs./2023/173. S.K.T. acknowledges the Indian Council of Medical Research, New Delhi for providing SRF. S.C. acknowledges the DBT-Ramalingaswamy fellowship, New Delhi. Used internal funds of the institute. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Funding Information:
Authors thank the Director, CSIR -IICT, Hyderabad, India, for providing the facilities and funding necessary for the conducting of this work. CSIR-IICT manuscript communication number: IICT/Pubs./2023/173 . S.K.T. acknowledges the Indian Council of Medical Research , New Delhi for providing SRF. S.C. acknowledges the DBT -Ramalingaswamy fellowship, New Delhi.
Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/10/1
Y1 - 2023/10/1
N2 - Aims: Acute lung inflammation, particularly acute respiratory distress syndrome (ARDS), is caused by a variety of pathogens including bacteria and viruses. β-Glucans have been reported to possess both anti-inflammatory and immunomodulatory properties. The current study evaluated the therapeutic effect of β-glucans on polyinosinic:polycytidylic acid (Poly(I:C)) induced lung inflammation in both hamster and mice models. Main methods: Poly(I:C)-induced ALI/inflammation models were developed in hamsters (2.5 mg/kg) and mice (2 mg/kg) by delivering the Poly(I:C) intratracheally, and followed with and without β-glucan administration. After treatment, lung mechanics were assessed and lung tissues were isolated and analyzed for mRNA/protein expression, and histopathological examinations. Key findings: Poly(I:C) administration, caused a significant elevation of inflammatory marker's expression in lung tissues and showed abnormal lung mechanics in mice and hamsters. Interestingly, treatment with β-glucan significantly (p < 0.001) reversed the Poly(I:C)-induced inflammatory events and inflammatory markers expression in both mRNA (IL-6, IL-1β, TNF-α, CCL2 and CCL7) and protein levels (TNF-α, CD68, myeloperoxidase, neutrophil elastase, MUC-5Ac and iNOS). Lung functional assays revealed that β-glucan treatment significantly improved lung mechanics. Histopathological analysis showed that β-glucan treatment significantly attenuated the Poly(I:C) induced inflammatory cell infiltration, injury and goblet cell population in lung tissues. Consistent with these findings, β-glucan treatment markedly reduced the number of neutrophils and macrophages in lung tissues. Our findings further demonstrated that β-glucan could reduce inflammation by suppressing the MAPK pathway. Significance: These results suggested that β-glucan may attenuate the pathogenic effects of Poly(I:C)-induced ALI/ARDS via modulating the MAPK pathway, indicating β-glucan as a possible therapeutic agent for the treatment of viral-pulmonary inflammation/injury.
AB - Aims: Acute lung inflammation, particularly acute respiratory distress syndrome (ARDS), is caused by a variety of pathogens including bacteria and viruses. β-Glucans have been reported to possess both anti-inflammatory and immunomodulatory properties. The current study evaluated the therapeutic effect of β-glucans on polyinosinic:polycytidylic acid (Poly(I:C)) induced lung inflammation in both hamster and mice models. Main methods: Poly(I:C)-induced ALI/inflammation models were developed in hamsters (2.5 mg/kg) and mice (2 mg/kg) by delivering the Poly(I:C) intratracheally, and followed with and without β-glucan administration. After treatment, lung mechanics were assessed and lung tissues were isolated and analyzed for mRNA/protein expression, and histopathological examinations. Key findings: Poly(I:C) administration, caused a significant elevation of inflammatory marker's expression in lung tissues and showed abnormal lung mechanics in mice and hamsters. Interestingly, treatment with β-glucan significantly (p < 0.001) reversed the Poly(I:C)-induced inflammatory events and inflammatory markers expression in both mRNA (IL-6, IL-1β, TNF-α, CCL2 and CCL7) and protein levels (TNF-α, CD68, myeloperoxidase, neutrophil elastase, MUC-5Ac and iNOS). Lung functional assays revealed that β-glucan treatment significantly improved lung mechanics. Histopathological analysis showed that β-glucan treatment significantly attenuated the Poly(I:C) induced inflammatory cell infiltration, injury and goblet cell population in lung tissues. Consistent with these findings, β-glucan treatment markedly reduced the number of neutrophils and macrophages in lung tissues. Our findings further demonstrated that β-glucan could reduce inflammation by suppressing the MAPK pathway. Significance: These results suggested that β-glucan may attenuate the pathogenic effects of Poly(I:C)-induced ALI/ARDS via modulating the MAPK pathway, indicating β-glucan as a possible therapeutic agent for the treatment of viral-pulmonary inflammation/injury.
UR - https://www.scopus.com/pages/publications/85168968898
UR - https://www.scopus.com/pages/publications/85168968898#tab=citedBy
U2 - 10.1016/j.lfs.2023.122027
DO - 10.1016/j.lfs.2023.122027
M3 - Article
C2 - 37597767
AN - SCOPUS:85168968898
SN - 0024-3205
VL - 330
JO - Life Sciences
JF - Life Sciences
M1 - 122027
ER -