MACROPHAGE INFLAMMATORY PROTEIN 2-Alpha (MIP-2) IN HIV PATIENTS LEADING TO LUNG INJURY AFTER <i>Pneumocystis jiroveci</i> INFECTION

Abstract

Introduction: Exuberant inflammation during Pneumonia caused by Pneumocystis jiroveci strongly promotes pulmonary injury in HIV patients and suggested caused by Macrophage Inflammatory Protein 2- Alpha (MIP-2) as a strong chemoattractant.Aims: To understanding the potential roles of MIP-2 in the pulmonary injury in HIV patients.Methods: All complete coding sequences of human MIP-2 deposited inGenBank were downloadedand subjected for bioinformatics analysis.Results: Human MIP-2 lacks the highly conserved purine at position -3 but possess many features of the consensus sequence. The consensus polyadenylation signal was present in the hu-MIP-2a cDNA at position 1182-1187of the 3' untranslated region followed by a poly(A) beginning at nucleotide 1202. The cysteine alignment and the presence of non conserved amino acid were defining the properties of chemokines in case of what substances that could be attracted. The mechanism of lung injury perhaps does not caused by alteration of MIP-2 directly.

Keywords: MIP-2, HIV, lung injury, Pneumocystis jiroveci 

References
Cao, X., W. Zhang, T. Wan, L. He, T. Chen, Z. Yuan, S. Ma, Y. Yu, and G. Chen. 2000. Molecular cloning and characterization of a novel CXC chemokine macrophage inflammatory protein-2g chemoattractant for human neutrophils and dendritic cells. JImmunol, vol. 165:2588-2595.
Connelly, S., and J.L. Manley. 1988. A functional mRNA polyadenylationsignal is required for transcription termination by RNA Polymerase II. Genes Dev, vol. 2:440-452.
Gigliotti, F., and T.W. Wright. 2005. Immunopathogenesis of Pneumocystis carinii Pneumonia. Expert Rev Mol Med,vol. 7:1-16.
Kapp, K., S. Schrempf, M.K. Lemberg, and B. Dobberstein. 2005.Post targeting functions of signal peptides. In: Zimmermann, R. Protein Trasnsport into the Endoplasmic Reticulum. Landes Bioscience. Austin.
Kelly, M.N., and J.E. Shellito. 2010. Current understanding of pneumocystis immunology. Future Microbiol, vol. 5:43-65.
Kungl, AJ. 2010. GAG Binding Protein. US Patent.

Maston, G.A., S.K. Evans, and M.R. Green. 2006. Transcriptional regulatoryelements in the humangenome. Annu Rev Genomics Hum Genet, vol. 7:29-59.

Morris, A., and K.A. Norris. 2012. Colonization by Pneumocystis jirovecii and its role in disease. ClinMicrobiol Rev, vol. 12:297-317.

Ng, P.C., and S. Henikoff. 2006. Predicting the effects ofamino acid substitutionson protein function. Annu Rev Genomics Hum Genet, vol. 7:61-80.

Proudfoot, N.J. 2011. Ending the message: Poly(A) signals then and now. Genes Dev, vol. 25:1770-1782.

Raiber, E., R. Kranaster, and S. Balasubramanian. 2012. A non-canonical DNA structure is a binding motif for the transcription factor SP1 in vitro. Nucleic Acids Res, vol. 40:1499- 1508.

Thomas, D.F., and A.H. Limper. 2007. Current Insights into the biology and pathogenesis of pneumocystis pneumonia. Nat Rev Microbiol, vol. 5:298-308.

Wang, J., F. Gigliotti, S. Maggirwar, C. Johnston, J.N. Finkelstein, T.W. Wright. 2005. Pneumocystis cariniiactivates the NF-kB signaling pathway in alveolar epithelial cells. Infect Immun, vol. 73:2766-2777.

Wasserman, W., and J. Fricket. 1998.Identification of regulatory regions which confer muscle- specific gene expression. J MolBiol, vol. 278:167-181.

Wasylyk, B., S.L. Hahn, and A. Giovane.1993.The Etsfamily of transcription factors.Eur J Biochem, vol. 211:7-18.