Osama Abdel‐Razek

SUNY Upstate Medical University

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Guirong Wang

SUNY Upstate Medical University

Robert N. Cooney

SUNY Upstate Medical University

Feng Ruan

Second Affiliated Hospital of Zhejiang University

Fengyong Yang

Jinan City People's Hospital

Junping Guo

Hangzhou Vocational and Technical College

G. Wang

SUNY Upstate Medical University

Qinghe Meng

SUNY Upstate Medical University

Yongan Xu

Second Affiliated Hospital of Zhejiang University

Jeffrey D. Amack

SUNY Upstate Medical University

Zhiyong Liu

Materials Science & Engineering

Cooperative Institutions

SUNY Upstate Medical University

Wuhan University

Renmin Hospital of Wuhan University

St. John's School

Syracuse University

Huazhong University of Science and Technology

SUNY Cortland

Suez Canal University

Fudan University

University of Maryland, Baltimore

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LIRAGLUTIDE ALLEVIATES ACUTE LUNG INJURY AND MORTALITY IN PNEUMONIA-INDUCED SEPSIS THROUGH REGULATING SURFACTANT PROTEIN EXPRESSION AND SECRETION

Shock (2023)

Junping Guo Xinghua Chen Cole Wang Feng Ruan Yunhe Xiong

ABSTRACT Glucagon-like peptide 1 (GLP-1) analogs are used to treat type 2 diabetes, and they can regulate insulin secretion, energy homeostasis, inflammation, and immune cell function. This study sought to determine whether the GLP-1 analog liraglutide exerts a beneficial action in an acute lung injury model of pneumonia-induced sepsis. Methods: Wild-type FVB/NJ mice (n = 114) were infected by intratracheal injection with Pseudomonas aeruginosa Xen5 (4 × 10 4 CFU/mouse) or an equal volume (50 μL) of saline (control) with or without a subcutaneous injection of liraglutide (2 mg/kg, 30 min after infection). Mice were killed 24 h after infection. Lung tissues and BALF were analyzed. In separate experiments, the dynamic growth of bacteria and animal mortality was monitored using in vivo imaging system within 48 h after infection. In addition, primary lung alveolar type II cells isolated from mice were used to study the mechanism of liraglutide action. Result: Liraglutide improved survival ( P < 0.05), decreased bacterial loads in vivo , and reduced lung injury scores ( P < 0.01) in septic mice. Liraglutide-treated mice showed decreased levels of inflammatory cells ( P < 0.01) and proinflammatory cytokines (TNF-α and IL-6) ( P < 0.01) in the lung compared with septic controls. Liraglutide significantly increased pulmonary surfactant proteins (SP-A and SP-B) expression/secretion ( P < 0.01) and phospholipid secretion ( P < 0.01) in vivo . Primary alveolar type II cells pretreated with liraglutide improved SP-A and SP-B expression after LPS exposure ( P < 0.01). Conclusion: Liraglutide attenuates mortality and lung inflammation/injury in pneumonia-induced sepsis. The increased surfactant expression/secretion and anti-inflammatory effects of liraglutide represent potential mechanisms by GLP-1 agonists potentiate host defense and maintain alveolar respiratory function in acute lung injury.

Proinflammatory cytokine

10.1097/shk.0000000000002285

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Citations (2)

Figure 6 C Effect of CMC 2.24 on oxidative stress.xlsx

Figshare (2020)

Osama Abdel‐Razek

The results showed significant increase in the levels of 8-Isoprostane in the BALFs of PM2.5 challenged mice (Panel C; p<0.05). However, the levels of 8-Isoprostane in the BALF were decreased substantially after CMC 2.24 treatment (p<0.01). Graphs represent the mean ± SEM. *p<0.05, **

10.6084/m9.figshare.12493454

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Bicyclic brominated furanones: A new class of quorum sensing modulators that inhibit bacterial biofilm formation

Bioorganic & Medicinal Chemistry (2014)

Sijie Yang Osama Abdel‐Razek Fei Cheng Debjyoti Bandyopadhyay Gauri Shetye

Virulence factor

10.1016/j.bmc.2014.01.004

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Citations (29)

Surfactant protein D attenuates acute lung and kidney injuries in pneumonia-induced sepsis through modulating apoptosis, inflammation and NF-κB signaling

Scientific Reports (2018)

Juan Du Osama Abdel‐Razek Qiao Shi Fengqi Hu Guohua Ding

Pneumonia and sepsis are major risk factors for acute kidney injury (AKI). Patients with pneumonia and AKI are at increased risk for morbidity and mortality. Surfactant protein D (SP-D) expressed in lung and kidney plays important roles in innate immunity. However, little is known about the role of organ-specific SP-D in the sepsis. The current study uses wild type (WT), SP-D knockout (KO), and humanized SP-D transgenic (hTG, lung-specific SP-D expression) mice to study organ-specific role of SP-D in pneumonia-induced sepsis. Analyses demonstrated differential lung and kidney injury among three-type mice infected with Pseudomonas aeruginosa. After infection, KO mice showed higher injurious scores in both lung and kidney, and decreased renal function than WT and hTG mice. hTG mice exhibited comparable lung injury but more severe kidney injury compared to WT mice. Increased renal tubular apoptosis, NF-κB activation and proinflammatory cytokines in the kidney of KO mice were found when compared with WT and hTG mice. Furthermore, in vitro primary proximal tubular epithelial cells from KO mice showed more apoptosis with higher level of activated caspase-3 than those from WT mice after LPS treatment. Collectively, SP-D attenuates AKI in the sepsis by modulating renal apoptosis, inflammation and NF-κB signaling.

Proinflammatory cytokine

10.1038/s41598-018-33828-7

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Citations (44)

Dynamical forces drive organ morphology changes during embryonic development

Raj Kumar Manna Emma M. Retzlaff Anna Maria Hinman Yiling Lan Osama Abdel‐Razek

Organs and tissues must change shape in precise ways during embryonic development to execute their functions. Multiple mechanisms including biochemical signaling pathways and biophysical forces help drive these morphology changes, but it has been difficult to tease apart their contributions, especially from tissue-scale dynamic forces that are typically ignored. We use a combination of mathematical models and

Morphology

10.1101/2024.07.13.603371

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Surfactant proteins and innate immunity of otitis media

Innate Immunity (2022)

Osama Abdel‐Razek Jason Audlin Dennis S. Poe Guirong Wang

Otitis media (OM) is the most common disease among young children and one of the most frequent reasons to visit the pediatrician. Development of OM requires nasopharyngeal colonization by a pathogen which must gain access to the tympanic cavity through the eustachian tube (ET) along with being able to overcome the defense mechanisms of the immune system and middle ear mucosa. OM can be caused by viral or bacterial infection. The three main bacterial pathogens are Streptococcus pneumoniae, nontypeable Haemophilus influenzae (NTHi), and Moraxella catarrhalis. Innate immunity is important in OM resolution as the disease occurs in very young children before the development of specific immunity. Elements of innate immunity include natural barriers and pattern recognition receptors such as Toll like receptors (TLRs), and Nod like receptors (NLRs). Surfactant proteins A (SP-A) and D (SP-D) act as pattern recognition receptors and are found in the lung and many other tissues including the ET and the middle ear where they probably function in host defense. Surfactant has a potential for use in the treatment of OM due to surface tension lowering function in the ET, and the possible immune functions of SP-D and SP-A in the middle ear and ET.

Eustachian tube

10.1177/17534259221123309

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Role of Surfactant Proteins A and D in Sepsis-Induced Acute Kidney Injury

Shock (2014)

Jiao Liu Osama Abdel‐Razek Zhiyong Liu Fengqi Hu Qingshan Zhou

Sepsis is a major cause of acute kidney injury (AKI) with high rates of morbidity and mortality. Surfactant proteins A and D (SP-A, SP-D) play a critical role in host defense and regulate inflammation during infection. Recent studies indicate SP-A and SP-D are expressed in the kidney. The current study examines the role of SP-A and SP-D in the pathogenesis of sepsis-induced AKI. Wild-type (WT) and SP-A/SP-D double-knockout (KO) C57BL/6 mice were treated by cecal ligation and puncture (CLP) or sham surgery. Histological, cellular, and molecular indices of kidney injury were investigated in septic mice 6 and 24 h after CLP. Twenty-four hours after CLP, kidney injury was more severe, renal function was decreased, and blood creatinine and blood urea nitrogen were higher in septic SP-A/SP-D KO mice (P < 0.05, versus septic WT mice). Kidney edema and vascular permeability were increased in septic SP-A/SP-D KO mice (P < 0.01, versus septic WT mice). Apoptotic cells increased significantly (P < 0.01) in the kidney of septic SP-A/SP-D KO mice compared with septic WT mice. Molecular analysis revealed levels of Bcl-2 (an inhibitor of apoptosis) were lower and levels of caspase 3 (a biomarker of apoptosis) were higher in the kidney of septic SP-A/SP-D KO mice (P < 0.01, versus septic WT mice). Furthermore, levels of nuclear factor κB and phosphorylated IκB-α increased significantly in the kidney of septic SP-A/SP-D KO mice compared with septic WT mice, suggesting SP-A/SP-D KO mice have a more pronounced inflammatory response to sepsis. We conclude SP-A and SP-D attenuate kidney injury by modulating inflammation and apoptosis in sepsis-induced AKI.

Pathogenesis

10.1097/shk.0000000000000270

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Citations (49)

Surfactant Protein D Dampens Lung Injury by Suppressing NLRP3 Inflammasome Activation and NF-κB Signaling in Acute Pancreatitis

Shock (2018)

Jia Yu Lan Ni Xiaoyi Zhang Jing Zhang Osama Abdel‐Razek

Severe acute pancreatitis (SAP) often causes acute lung injury (ALI) by systemic inflammatory response. Surfactant protein D (SP-D) plays critical roles in host defense and inflammation regulation. NLRP3 inflammasomes and NF-κB signaling are key regulators in innate immunity and inflammation. We hypothesized that SP-D attenuates ALI by suppressing NLRP3 inflammasome and NF-κB activation.Wild-type C57BL/6 (WT), SP-D knockout (KO), and humanized transgenic SP-D (hTG) mice were used in this study. SAP was induced by administration of one-dose lipopolysaccharide (10 mg/kg) and 6 hourly intraperitoneal injections of cerulein (Cn) (100 μg/kg). Animals were killed 6 and 24 h after first Cn treatment. Histopathologic changes in pancreas and lung were assessed by light and electron microscopes. Serum amylase, IL-1β, IL-6, and MCP-1 levels were determined by kit/ELISA. NLRP3 inflammasome, NF-κB, and MPO activations were analyzed by western blotting and immunofluorescence.KO mice showed more severe pancreatic and lung injury than WT mice in SAP. hTG mice exhibited similar degree in lung injury as WT mice. Mitochondrial and rough endoplasmic reticulum damages, autophagosome formation were observed in the alveolar type II and acinar cells of SAP mice. SAP KO mice had increased bronchoalveolar lavage fluid inflammatory cells, higher levels of serum IL-1β, IL-6, and MCP-1 than SAP WT and hTG mice. Levels of NLRP3 inflammasome (NLRP3, ASC, and Caspase-1) and NF-κB activation in SAP KO mice were higher than SAP WT and hTG mice.SP-D exerts protective effects against ALI via suppressing NLRP3 inflammasome and NF-κB activation in experimental SAP.

10.1097/shk.0000000000001244

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Regulatory Roles of Human Surfactant Protein B Variants on Genetic Susceptibility to Pseudomonas Aeruginosa Pneumonia-Induced Sepsis

Shock (2019)

Fengyong Yang Jing Zhang Yi Yang Feng Ruan Xinghua Chen

Surfactant protein B (SP-B) is essential for life and plays critical roles in host defense and lowering alveolar surface tension. A single-nucleotide polymorphism (SNP rs1130866) of human SP-B (hSP-B) alters the N-linked glycosylation, thus presumably affecting SP-B function. This study has investigated the regulatory roles of hSP-B genetic variants on lung injury in pneumonia-induced sepsis.Wild-type (WT) FVB/NJ and humanized transgenic SP-B-T and SP-B-C mice (expressing either hSP-B C or T allele without mouse SP-B gene) were infected intratracheally with 50 μL (4 × 10 colony-forming units [CFUs]/mouse) Pseudomonas aeruginosa Xen5 or saline, and then killed 24 or 48 h after infection. Bacterial dynamic growths were monitored from 0 to 48 h postinfection by in vivo imaging. Histopathological, cellular, and molecular changes of lung tissues and bronchoalveolar lavage fluid (BALF) were analyzed. Surface tension of surfactants was determined with constrained drop surfactometry.SP-B-C mice showed higher bioluminescence and CFUs, increased inflammation and mortality, the higher score of lung injury, and reduced numbers of lamellar bodies in type II cells compared with SP-B-T or WT (P < 0.05). Minimum surface tension increased dramatically in infected mice (P < 0.01) with the order of SP-B-C > SP-B-T > WT. Levels of multiple cytokines in the lung of infected SP-B-C were higher than those of SP-B-T and WT (P < 0.01). Furthermore, compared with SP-B-T or WT, SP-B-C exhibited lower SP-B, higher NF-κB and NLRP3 inflammasome activation, and higher activated caspase-3.hSP-B variants differentially regulate susceptibility through modulating the surface activity of surfactant, cell death, and inflammatory signaling in sepsis.

Ex vivo

10.1097/shk.0000000000001494

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Differences in expression of the human differences in expression of the human SFTPB variant determine susceptibility to Staphylococcus aureus infection in lung

Journal of Critical Care (2015)

Jiao Liu Zhiyong Liu Osama Abdel‐Razek Sara Javidiparsijani Yunhe Xiong

Brier score

SOFA score

Coronary care unit

10.1016/j.jcrc.2015.04.018

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