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John I. Gallin, M.D.
Building 10-CRC, Room 6-2551
10 Center Drive
Bethesda, MD 20892-1504
Phone: 301-496-4114
Fax: 301-402-0244

Douglas B. Kuhns, Ph.D., Head, Neutrophil Monitoring Lab
Phone: 301-846-6378

Laboratory of Host Defenses

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Photo of John I. Gallin

John I. Gallin, M.D.

Chief, Clinical Pathophysiology Section, LHD
Director, Clinical Center, National Institutes of Health (NIH)

Major Areas of Research

  • Inflammation
  • Phagocyte dysfunction




Program Description

The mission of the Clinical Pathophysiology Section is to study the genetic causes and the biological consequences of inborn diseases of phagocytic blood cells.

illustrations of diseases of monocytes and neutrophils
Figure 1. The neutrophil and monocyte are the most abundant white blood cells in the circulation. Upon stimulation, they adhere to the endothelium and migrate into the tissues, where they seek and destroy pathogens. Disorder of cell signaling, granules, and oxygen metabolism have been described. The various diseases of monocytes and neutrophils studied by the Clinical Pathophysiology Section, including leukocyte adhesion deficiency, IRAK4-deficiency, NEMO-deficiency, Job’s syndrome, secondary granule deficiency, Chediak-Higashi syndrome, myeloperoxidase deficiency, and all genotypes of chronic granulomatous disease (CGD).
Credit: NIAID

Among these, chronic granulomatous disease (CGD) has been our major focus. CGD occurs in patients whose phagocytes (neutrophils and monocytes) are unable to generate antimicrobial levels of reactive oxygen species (e.g., superoxide anion) due to mutations in components of the NADPH oxidase as shown below.

illustration of amino acid mutations
Figure 2. The amino acid mutations in components of the NADPH oxidase that have been associated with chronic granulomatous disease (See Kuhns et al., NEJM 2010).
Credit: NIAID

Without sufficient production of superoxide anion, a key mediator of host defense, these patients suffer from life-threatening bacterial and fungal infections as well as tissue granuloma formation and other inflammatory diseases. Our section studies host and microbial determinants of pathogenesis by fungal (e.g., Aspergillus fumigatus) and bacterial (e.g., Granulibacter bethesdensis) causes of infection in CGD patients. We also perform clinical and laboratory studies of patients with CGD or other immunodeficiencies shown above to better understand the regulation of inflammation and the immune system in human subjects.


Dr. Gallin received his medical training at Cornell University Medical College in New York City followed by residency in internal medicine at Bellevue Hospital. In 1971, he first came to NIH as a clinical associate. In 1974 he served as senior chief resident in medicine at Bellevue Hospital before returning to NIH in 1976 as a senior investigator. Dr. Gallin has served as scientific director of the NIAID intramural research program (1985–1994) and as chief of the Laboratory of Host Defenses (1991–2003). Since 1994, Dr. Gallin has been director of the NIH Clinical Center. Dr. Gallin has numerous honors, including being a master of the American College of Physicians and being elected to membership of the Association of American Physicians, the American Society of Clinical Investigation, the American Association of Immunologists, and the Institute of Medicine of the National Academy of Sciences.

Research Group

photo of group members
Left to right: Douglas Kuhns, Ph.D.; Jessica Chu, Ph.D.; Kol Zarember, Ph.D.; John Gallin, M.D.; Helen Song, B.S.

Closely associated with CPS is the Neutrophil Monitoring Laboratory (NML), a CLIA-certified facility in Frederick, Maryland, that supports the clinical and basic research of the NIAID Laboratory of Host Defenses and the NIAID Laboratory of Clinical Infectious Diseases. NML is headed by Douglas Kuhns, Ph.D. (contractor, SAIC-Frederick, Inc.), and performs genetic and functional studies on cells isolated from patients with recurrent bacterial and fungal infections, as well as patients with abnormal inflammatory responses.

Selected Publications

Zarember KA, Marshall-Batty KR, Cruz AR, Chu J, Fenster ME, Shoffner AR, Rogge LS, Whitney AR, Czapiga M, Song HH, Shaw PA, Nagashima K, Malech HL, DeLeo FR, Holland SM, Gallin JI, Greenberg DE. Innate immunity against Granulibacter bethesdensis, an emerging gram-negative bacterial pathogen. Infect Immun. 2012 Mar;80(3):975-81

Gallin JI. The NIH Clinical Center and the future of clinical research. Nat Med. 2011 Oct 11;17(10):1221-3.

Kuhns DB, Alvord WG, Heller T, Feld JJ, Pike KM, Marciano BE, Uzel G, DeRavin SS, Priel DA, Soule BP, Zarember KA, Malech HL, Holland SM, Gallin JI. Residual NADPH oxidase and survival in chronic granulomatous diseaseN Engl J Med. 2010 Dec 30;363(27):2600-10.

Roos D, Kuhns DB, Maddalena A, Roesler J, Lopez JA, Ariga T, Avcin T, de Boer M, Bustamante J, Condino-Neto A, Di Matteo G, He J, Hill HR, Holland SM, Kannengiesser C, Köker MY, Kondratenko I, van Leeuwen K, Malech HL, Marodi L, Nunoi H, Stasia MJ, Ventura AM, Witwer CT, Wolach B, Gallin JI. Hematologically important mutations: X-linked chronic granulomatous disease (third update). Blood Cells Mol Dis. 2010 Oct 15;45(3):246-65.

De Ravin SS, Zarember KA, Long-Priel D, Chan KC, Fox SD, Gallin JI, Kuhns DB, Malech HL. Tryptophan/kynurenine metabolism in human leukocytes is independent of superoxide and is fully maintained in chronic granulomatous diseaseBlood. 2010 Sep 9;116(10):1755-60.

Singh A, Zarember KA, Kuhns DB, Gallin JI. Impaired priming and activation of the neutrophil NADPH oxidase in patients with IRAK4 or NEMO deficiencyJ Immunol. 2009 May 15;182(10):6410-7.

Visit PubMed for a complete publication listing.

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Last Updated June 06, 2011

Last Reviewed June 06, 2011