Education

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Employment History

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Teaching

Associate Professor, Microbiology and Immunology, Touro University Nevada

Course Director and lecturer, Infection and Immunity (BSCI-610N) for 1st year DO students (2004- )

Course Director and lecturer, Medical Microbiology and Immunology-I (BSCI-624N) for 2nd year DO students (2004- )

Course Director and lecturer, Medical Microbiology and Immunology-II (BSCI-636N) for 2nd year DO students (2004- )

Course Director and lecturer, Clinical Microbiology and Immunology (PA658) for PA students (2004- 2006)

Course Director and lecturer, Immunology (PA659) for PA students (2006- )

Course Director and lecturer, Medical Microbiology (PA658) for PA students (2006- )

Failitator, Lab Diagnosis (BSCI 639-N) for 2nd year DO students (2006- )

Facilitator, PBL sessions for 1st year DO students (2004- present)

Lecturer, Clinical System (PRCR 641-N) for 2nd year DO students (2005- )

Lecturer, Pharmacology (BSCI 647-N) for 2nd year DO students (2006- )

Assistant Professor, College of Life Sciences, University of Nevada Las Vegas

Lecturer, Microbial System (BIOL 351X), for UNLV Life Science graduate/undergraduate students (2006- )

Research Associate, University of Kentucky, Department of Internal Medicine and Microbiology, Immunology and Molecular Genetics

Lecturer, Basic Science Lecture Series, offered to the clinicians in the Department of Internal Medicine, University of Kentucky (1999-2004)

Teaching Assistant, University of Ryukyus, College of Medicine, Japan

Microbiology and Immunology Graduate Course (1995-1998)

Teaching Assistant, University of Ryukyus, College of Medicine, Japan

Epidemiology Graduate Course (1993-1994)

Assistant Surgeon, Dhaka Medical College Hospital, Dhaka, Bangladesh

Clinical lecturer to resident physicians and medical students (1988-1992)

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Research Interests

Research Interest

I. Role of dendritic cells in inadequate immune responses to P. carinii (PC) in neonates
We have reported that neonates have a predominantly defective lung environment rather than inefficient immune effector cells accountable for inadequate immune response (Garvy & Qureshi, J. Immunol., 2000; Qureshi & Garvy, J. Immunol., 2001, Qureshi et. al., J. Immunol., 2003). However, it is not clearly understood as to whether other components of neonatal lung environment have adult-like functioning. Appropriate antigen presentation by professional antigen presenting cells (APCs) is a prerequisite for an effective immune response. Dendritic cells are the major APC in the respiratory tract. Inefficient dendritic cell (DC) function in the neonatal respiratory tract may be involved in defective neonatal host-responses to respiratory pathogens including PC. The goal of these studies is to address the hypothesis that inefficient antigen uptake and migration of DCs to the draining lymph nodes as well as simultaneous maturation is inefficient in neonates resulting in inefficient proliferation and activation of effector T cells and delayed resolution of PC pneumonia (PCP). The information regarding differential antigen uptake, migration ability and the dynamics of chemokine receptor expression of neonatal and adult DCs would help us better understand some important differences in the initiation of immune responses in the two age groups. A complete understanding of the role of DC in neonatal immune responses may lead to development of new form of immunotherapies, including DC-based vaccine strategies, which may be used as an adjunct to existing chemotherapy to protect the vulnerable neonates from respiratory pathogens.

II. Concurrent infection with P. carinii (PC) and CMV in mice
Despite the practice of antimicrobial prophylaxis, cytomegalovirus (CMV) and PC pneumonia (PCP) are both leading causes of mortality and morbidity in patients with immunocompromised states resulting from malignancies, solid organ and bone marrow transplants, or AIDS. In addition, newborns with congenital or perinatal CMV infection also suffer from concomitant PCP. The interaction of these pathogens and their effects on host immune responses is not clearly understood. Therefore, it is important to better understand the pathophysiology of PC and CMV dual infection. CMV modulates host-immune responses by suppressing helper T cell function critical for PCP resolution, as well as APC functions. Therefore, the goal of these studies is to test the working hypothesis that murine CMV (MCMV)-induced immunomodulation exacerbates PCP progression through delayed clearance of PC during concurrent PC and MCMV infection. These experiments will provide insight into the interaction of PC and MCMV and its effect on host responses, and can serve as a basis for developing new strategies to protect and treat immunocompromised patients susceptible to PC and CMV infections.

III. RSV-induced polarization of dendritic cells and susceptibility to asthma
Respiratory syncytial virus (RSV)-infected children becomes susceptible to develop asthma in later life. The exact mechanism for this post-RSV susceptibility to asthma is not clearly understood. Clinical and animal studies have shown that RSV infections induce significantly high production of Th2 cytokines. This Th2 response is extrapolated in explaining the hyperresponsiveness of the RSV-infected lungs. In this regard, it is important to mention that a predominant Th2 environment generally prevails in the lungs of neonates and young infants. Further, induction of immune response is largely dependent on the antigen presenting cell (APC). Dendritic cells are the major APC in the respiratory tract. Dendritic cells always do not induce immunity; rather sometimes induce tolerance response. In humans two subsets of DC, myeloid DCs (mDCs) and plasmacytoid DCs (pDCs), have been identified. mDCs drive a Th1 type of immune response; hence type 1 DCs (DC1). The other types of DCs, the pDCs, is also called Type 2 DCs (DC2) as they induce Th2 type of response. Therefore, the goal of the present study is to identify whether RSV infection polarizes differentiation of respiratory tract DC to pDCs and hence make the host susceptible to develop an enhancedTh2 response to innocuous antigens leading to asthma. A mouse model of RSV infection with exposure to asthma inducing allergen, as well as, human RSV patients will be used for these studies. This study intends to establish the polarization of DC towards pDC as a parameter in clinical practice for determining susceptibility to asthma. It is very likely that reversal of this skewing of DC population by immunomodulators will change the susceptibility of the RSV-infected patients to develop asthma. We intend to investigate this possibility in our future studies.

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Honors & Awards

Teacher of the Year, Touro University Nevada, College of Osteopathic Medicine (2007)

Final nominee for Northup Educator of the Year, Student Osteopathic Medical
Association (2007)

Teacher of the Year, Touro University Nevada, College of Osteopathic Medicine (2006)

Research Fellowship award, American Lung Association (2003)

Research Fellowship award, American Lung Association (2002)

ASM Sustaining Membership Grant, American Society for Microbiology (1999)

ASM Sustaining Membership Grant, American Society for Microbiology (1998)

MONBUSHO Scholarship, Ministry of education, Govt. of Japan (1993-1999)

National Board Scholarship for medical students, Ministry of Education, Govt. of Bangladesh (1980-1985)

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Publications

Qureshi MH, Garvy BA, Pomeroy C, Inayat MS, Oakley OR. A murine model of dual
infection with cytomegalovirus and Pneumocystis carinii: Effects of virus-induced immunomodulation on disease progression. Virus Res. 2005; 114(1-2):35-44.

Qureshi MH, Garvy BA. Modulation of proinflammatory responses to Pneumocystis carinii f. sp. muris in neonatal mice by granulocyte-macrophage colony-stimulating factor and IL-4: Role of APCs. J Immunol. 2005; 174(1): 441-8.

Qureshi MH, Harmsen AH, Garvy BA. IL-10 modulates host responses and lung damage induced by Pneumocystis carinii infection. J. Immunol. 2003; 170(2): 1002-
09.

Qureshi MH, Cook-mills J, Doherty D, Garvy BA. TNF--dependent ICAM-1 and
VCAM-1 mediated immune responses are delayed in neonates infected with Pneumocystis carinii. J. Immunol. 2003; 171(9): 4700-4707.

Kawakami K, Koguchi Y, Qureshi MH, Zhang T, Kinjo Y, Yara S, Uezu K, Shibuya
K, Naoe S, Saito A.Anti-CD11b monoclonal antibody suppresses brain dissemination of Cryptococcus neoformans in mice. Microbiol Immunol. 2002; 46(3):181-6.

Qureshi MH, Garvy BA. Neonatal T Cells in an Adult Lung Environment Are
competent to Resolve Pneumocystis carinii Pneumonia. J Immunol. 2001; 166(9): 5704-11.

Qureshi MH, Garvy BA. IFN- regulates host-response to Pneumocystis carinii infection via optimizing the induction of cytokines, chemokines and corresponding receptors. FASEB J. 2001; 15 (4): A689.

Kawakami K, Koguchi Y, Qureshi MH, Yara S, Kinjo Y, Uezu K, Saito A. NK cells eliminate Cryptococcus neoformans by potentiating the fungicidal activity of macrophages rather than by directly killing them upon stimulation with IL-12 and IL-18. Microbiol Immunol. 2000; 44(12): 1043-50.

Kawakami K, Koguchi Y, Qureshi MH, Yara S, Kinjo Y, Miyazato A, Nariuchi H,
Saito A. Circulating soluble CD4 directly prevents host resistance and delayed-type
hypersensitivity response to Cryptococcus neoformans in mice. Microbiol Immunol.
2000; 44(12): 1033-41.

Garvy BA, Qureshi MH. Delayed inflammatory response to Pneumocystis carinii infection in neonatal mice is due to an inadequate lung environment. J Immunol. 2000; 165(11): 6480-6.

Kawakami K, Koguchi Y, Qureshi MH, Miyazato A, Yara S, Kinjo Y, Iwakura Y, Takeda K, Akira S, Kurimoto M, Saito A. IL-18 contributes to host resistance against infection with Cryptococcus neoformans in mice with defective IL-12 synthesis through induction of IFN- production by NK cells. J Immunol. 2000; 165(2): 941-7.

Kawakami K, Koguchi Y, Qureshi MH, Kinjo Y, Yara S, Miyazato A, Kurimoto M,
kira S, Saito A. Reduced host resistance and Th1 response to Cryptococcus neoformans in interleukin-18 deficient mice. FEMS Microbiol Lett. 2000; 186(1):121-6.

Kawakami K, Qureshi MH, Zhang T, Koguchi Y, Yara S, Takeda K, Akira S,
Kurimoto M, Saito A. Involvement of endogenously synthesized interleukin (IL)-18 in the protective effects of IL-12 against pulmonary infection with Cryptococcus neoformans in mice. FEMS Immunol Med Microbiol. 2000; 27(3): 191-200.

Qureshi MH, Garvy BA. Inadequate immune response in neonates against Pneumocystis carinii infection is due to factors other than immature lymphocytes. FASEB J. 2000; 14(6):A953.

Garvy BA, Qureshi MH. Insufficient environment for lymphocyte migration into the lungs of neonatal mice in response to Pneumocystis carinii. FASEB J. 2000; 14(6):A1028.

Kawakami K, Qureshi MH, Zhang T, Saito A. Interleukin-4 weakens host resistance to pulmonary and disseminated cryptococcal infection caused by combined treatment with IFN- inducing cytokines. Cell. Immunol. 1999; 197 (1): 55- 61.

Kawakami K, Shibuya K, Qureshi MH, Zhang T, Koguchi Y, Tohyama M, Xie Q, Naoe S, Saito A. Chemokine responses and accumulation of inflammatory cells in the lungs of mice infected with highly virulent Cryptococcus neoformans: effects of interleukin-12. FEMS Immunol Med Microbiol. 1999; 25(4):391-402.

Kawakami K, Qureshi MH, Zhang T, Koguchi Y, Shibuya K, Naoe S, Saito A. Interferon-gamma (IFN-)-dependent protection and synthesis of chemoattractants for mononuclear leucocytes caused by IL-12 in the lungs of mice infected with Cryptococcus neoformans. Clin Exp Immunol. 1999; 117(1): 113-22.

Kawakami K, Qureshi MH, Koguchi Y, Nakajima K, Saito A. Differential effect of
Cryptococcus neoformans on the production of IL-12p40 and IL-10 by murine
Macrophages stimulated with lipopolysaccharide and gamma interferon. FEMS Microbiol Lett. 1999; 175(1): 87-94.

Kawakami K, Qureshi MH, Koguchi Y, Zhang T, Okamura H, Kurimoto M, Saito A. Role of TNF- in the induction of fungicidal activity of mouse peritoneal exudates cells against Cryptococcus neoformans by IL-12 and IL-18. Cell Immunol. 1999;193(1): 9-16.

Chinen T, Qureshi MH, Koguchi Y, Kawakami K. Candida albicans suppresses nitric oxide (NO) production by interferon-gamma (IFN-) and lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages. Clin Exp. Immunol. 1999;115(3):491-7.

Qureshi MH, Zhang T, Koguchi Y, Nakashima K, Okamura H, Kurimoto M, Kawakami K. Combined effects of IL-12 and IL-18 on the clinical course and local cytokine production in murine pulmonary infection with Cryptococcus neoformans.
Eur J Immunol. 1999; 29(2):643-9.

Kawakami K, Qureshi MH, Zhang T, Okamura H, Kurimoto M, Saito A. IL-18 protects mice against pulmonary and disseminated infection with Cryptococcus neoformans by inducing IFN-gamma production. J Immunol. 1997; 159(11): 5528-

Xie Q, Kawakami K, Kudeken N, Zhang T, Qureshi MH, Saito A. Different susceptibility of three clinically isolated strains of Cryptococcus neoformans to the fungicidal effects of reactive nitrogen and oxygen intermediates: possible relationships with virulence. Microbiol Immunol. 1997; 41(9):725-31.

Kawakami K, Zhang T, Qureshi MH, Saito A. Cryptococcus neoformans inhibits nitric oxide production by murine peritoneal macrophages stimulated with interferon-gamma and lipopolysaccharide. Cell Immunol. 1997; 180(1): 47-54.

Zhang T, Kawakami K, Qureshi MH, Okamura H, Kurimoto M, Saito A.
Interleukin-12 (IL-12) and IL-18 synergistically induce the fungicidal activity of murine peritoneal exudate cells against Cryptococcus neoformans through production of gamma interferon by natural killer cells. Infect Immun. 1997; 65(9): 3594-9.

Kawakami K, Qifeng X, Tohyama M, Qureshi MH, Saito A. Contribution of tumour necrosis factor-alpha (TNF-) in host defence mechanism against Cryptococcus neoformans. Clin Exp Immunol. 1996; 106(3): 468-74.

Qureshi MH, Katoh T, Iibuchi Y. Sex differential in life expectancy in Japan and Scotland: age and causes of death. Acta Med Okayama. 1995 Apr; 49(2): 97-106.

The Neonatal Period, Garvy, BA and Qureshi, MH, in Pneumocystis carinii Pneumonia, 3rd edition, pp. 183-203. Eds. P. Waltzer and M. Cushion. Marcel Dekker, NY.

Interleukin 12 (IL-12) in host-defense and immunotherapy, Qureshi MH, in Immunomodulators as Promising Therapeutic Agents Against Infectious Diseases, pp. 55-87. Eds. Kazuyoshi Kawakami and David A. Stevens. Research Signpost, India.

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