Respiratory Tract Infections; Pulmonary Disease, Chronic Obstructive
Our group is committed to innovative and cutting-edge basic, translational and clinical research that will further our understanding of pulmonary infections and lead to effective diagnosis and treatment. Current therapies for pulmonary infections have largely focused on the use of antibiotics and have led to the rapid emergence of drug resistance and hypervirulent strains. We will address current priorities in novel strategies in studying the host and the pathogen for both acute and chronic pulmonary infections. The research endeavors are aimed at delineating the basic mechanisms by which pulmonary pathogens cause disease as well as applying scientific advances to promote patient diagnosis and treatment
Our work is focused in both explorative and targeted research relevant to pulmonary infection and immunity in 3 specific areas:
(1) To explore the basic science of key host-microbe molecular and cellular interactions in the lung;
(2) To investigate and define the mechanisms of infections which either cause or exacerbate acute / chronic lung diseases using both basic and translational approaches;
(3) To utilize and develop novel technologies that will make it possible to better diagnose and treat pernicious lung infections.
- Berical AC, Harris D, Dela Cruz CS, Possick JD. Ann Am Thorac Soc. 2016 Apr 18.
- Yoon CM, Nam M, Oh YM, Dela Cruz CS, Kang MJ. J Innate Immun. 2016;8(2):121-8. doi: 10.1159/000441299. Epub 2015 Nov 5.
- Wang J, Liu W, Marion C, Singh R, Andrews N, Lee CG, Elias JA, Dela Cruz CS. Am J Respir Cell Mol Biol. 2015 Dec;53(6):822-33. doi: 10.1165/rcmb.2014-0448OC.
- Dela Cruz CS, Liu W, He CH, Jacoby A, Gornitzky A, Ma B, Flavell R, Lee CG, Elias JA. Chitinase 3-like-1 (Chi3l1) regulation of Streptococcus pneumoniae lung infection. 2012. Cell Host and Microbe, 12:23-46.
- Ma B, Dela Cruz CS, Hartl D, Kang MJ, Takyar S, Homer RJ, Lee CG, Elias JA. 2011. RIG-like helicase innate immunity inhibits vascular endothelial growth factor tissue responses via a type I IFN-dependent mechanism. Am J Respir Crit Care Med, 183(10):1322-35
- Matsuura H, Hartl D, Kang MJ, Dela Cruz CS, Koller B, Chupp GL, Homer RJ, Zhou Y, Cho WK, Elias JA, Lee CG. 2011. Role of breast regression protein-39 in the pathogenesis of cigarette smoke-induced inflammation and emphysema. Am J Respir Cell Mol Biol, 44(6):777-86.
- Lee CG, Da Silva CA, Dela Cruz CS, Ahangari F, Ma B, Kang MJ, He CH, Takyar S, Elias JA. 2011. Role of chitin and chitinase/chitinase-like proteins in inflammation, tissue remodeling, and injury. Annu Rev Physiol, 73:479-501.
- Dela Cruz CS, Kang MJ, Cho WK, Lee CG. 2010. Transgenic Modeling of Cytokine Polarization in the Lung, Immunology, 132(1):9-17.
- Lee CG, Da Silva C, Dela Cruz CS, Ahangari F, Ma B, Kang MJ, He CH, Takyar S, Elias JA. Role of chitin, chitinase/chitinase-like proteins (C/CLP) in inflammation, tissue remodeling and injury, 2010. Annual Review of Physiology, Feb 19, Epub.
- Kang MJ, Lee CG, Dela Cruz CS, Enelow R and Elias JA. Cigarette Smoke Selectively Enhances Viral PAMP and Virus-Induced Innate Immune Responses and Emphysematous Tissue Destruction in the Murine Lung. J Clin Invest. 2008. 118:2771-2784.
- Dela Cruz CS, Viswanathan SR, El-Guindy AS, Shedd D, Miller G. Complex N-linked glycans on Asn-89 of Kaposi sarcoma herpes virus-encoded interleukin-6 mediate optimal function by affecting cytokine protein conformation. J Biol Chem. 2009. 284(43):29269-82.
- Dela Cruz CS, Lee Y, Viswanathan SR, El-Guindy AS, Gerlach J, Nikiforow S, Shedd D & Miller G. N-linked Glycosylation is Required for Optimal Function of Kaposi’s Sarcoma Herpesvirus Encoded, but not Cellular, IL-6. J Exp Med. 2004, 199: 503-514.
- Popov I, Dela Cruz CS, Barber BH, Chiu B & Inman RD. Breakdown of CTL tolerance to self HLA-B*2705 induced by exposure to Chlamydia trachomatis. J Immunol. 2002, 169:4033-8.
- Arthos J, Cicala C, Steenbeke TD, Chun TW, Dela Cruz C, Hanback DB, Khazanie P, Nam D, Schuck P, Selig SM, Van Ryk D, Chaikin MA & Fauci AS.(2002) Biochemical and biological characterization of a dodecameric CD4-Ig fusion protein: implications for therapeutic and vaccine strategies.