Program Schedule

Innate Pulmonary Response to Community-Acquired Pneumonia (CAP) in Patients with Chronic Obstructive Pulmonary Disease (COPD): Results from the Community-Acquired Pneumonia Inflammatory Study Group (CAPISG)

Session: Poster Abstract Session: Biomarkers of Immune Responses
Saturday, October 11, 2014
Room: The Pennsylvania Convention Center: IDExpo Hall BC
  • Poster PNA and COPD.CAPISG . IDWeek 2014 10 3 2014.pdf (621.2 kB)
  • Background:

    Patients with COPD have chronic airway inflammation characterized by increased cytokine levels and neutrophil activation. It is not well defined if these chronic inflammatory changes in the airway may impair the innate pulmonary response during an episode of CAP. The objective of this study was to compare cytokine production and neutrophil function in patients with CAP with and without COPD. 


    Blood samples were collected from 40 patients diagnosed with CAP upon admission to the hospital. The plasma levels of 10 different cytokines and chemokines were measured, as well as the peripheral blood neutrophil function. Patients were grouped according to the presence of COPD [CAP-COPD (+) vs. CAP-COPD (-)]. The Mann-Whitney U test was used to compare cytokine and chemokine levels between the CAP-COPD (+) and CAP-COPD (-) groups.


    A total of 14 CAP-COPD (+) and 26 CAP-COPD (-) patients were enrolled. Median (interquartile range) CD35 expression was 163 (111) in CAP-COPD (+) and 127 (101) in CAP-COPD (-) (P=0.238). CD66b expression was 62 (44) in CAP-COPD (+) and 63 (24) in CAP-COPD (-) (P=0.847). Ph-Sa was 837 (810) in CAP-COPD (+) and 913 (880) in CAP-COPD (-) (P=0.713). H2O2 production was 536 (480) in CAP-COPD (+) and 726 (406) in CAP-COPD (-) (P=0.494). The cytokine and chemokine levels didn’t show significant differences between groups.


    The innate pulmonary response during an episode of CAP measured by cytokine production and neutrophil function is not different in patients with or without COPD. These data support the clinical concept that COPD is not a risk factor to poor outcomes in patients with CAP.

    Lisandra Rodriguez Hernandez, MD1, Jorge Perez San Juan, MD1, Robert Kelley, PhD1, Timothy L. Wiemken, PhD, MPH, CIC1, Rafael Fernandez-Botran, PhD2, Martin Gnoni, MD1, Paula Peyrani, MD1, Jose Bordon, MD, PhD3, Madhavi Rane, PhD4, Forest Arnold, DO1, Julio a. Ramirez, MD1 and Silvia Uriarte, PhD5, (1)Division of Infectious Diseases, University of Louisville, Louisville, KY, (2)Pathology and Laboratory Medicine, University of Louisville, Louisville, KY, (3)Section of Infectious Diseases, Providence Hospital, Washington, DC, (4)Division of Nephrology, University of Louisville, Louisville, KY, (5)Kidney Disease Program, University of Louisville, Louisville, KY


    L. Rodriguez Hernandez, None

    J. Perez San Juan, None

    R. Kelley, None

    T. L. Wiemken, None

    R. Fernandez-Botran, None

    M. Gnoni, None

    P. Peyrani, None

    J. Bordon, None

    M. Rane, None

    F. Arnold, None

    J. A. Ramirez, None

    S. Uriarte, None

    Findings in the abstracts are embargoed until 12:01 a.m. EDT, Oct. 8th with the exception of research findings presented at the IDWeek press conferences.

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