Clark M. Blatteis, Ph.D.
1954 B.A., Rutgers University , NCAS, Newark, New Jersey
1955 M.Sc., University of Iowa, Iowa City, Iowa
1957 Ph.D., University of Iowa, Iowa City, Iowa
1968 - OAS (Peru) Fellow
1975, 1994 - Senior Fulbright-Hays Scholar (Peru)
1979, 1981 - DFG (Germany) Fellow
1983 - CSIRO (Australia) Fellow
1983-1988 - Member International Union of Physiological Sciences Commission on Thermal Physiology
1988-1996 - Chairman International Union of Physiological Sciences Commission on Thermal Physiology
1994, 1998 - Professor honoris causa, National Univ. of Trujillo, Trujillo, Peru and Peruvian Univ. Cayetano Heredia, Lima, Peru
1998 - Honorary President, Peruvian Physiological and Pathophysiological Society
2003 - American Physiological Society-Environmental and Exercise Physiology Section Honor Award
2007 - Inductee, Living History of Physiology
For almost 35 years, our lab has been principally engaged in elucidating the mechanisms that underlie the febrile response to infection. The focus of our research has been on the interactions between the immune and nervous systems that initiate this response.
Fever is one among an array of non-specific innate immune, endocrine, metabolic, behavioral, and other responses to the entry into the body of infectious microorganisms or their products, designed to defend the afflicted host from the deleterious effects of the invading pathogens. These responses are collectively termed the acute-phase reaction (APR). The APR is thus a physiological, not a pathological, response. In its simplest terms, the febrile response per se is characterized by a rise of the body core temperature (Tc). It is, thus, a thermoregulatory response that involves a complete, prototypic reflex arc ? sensory signaling, central integration, and effector mechanisms.
Over the years, we have, in turn, described the ontogeny of fever and the change in effector mechanisms that occurs over the first month of post-natal life, localized the several brain sites that mediate the febrile response, and eventually characterized the complete loop of fever production, from the moment the pyrogenic material enters the body until the febrile response is initiated. In more recent years, our efforts have been concentrated most heavily on resolving this latter issue. Thus, we have identified various endogenous factors liberated in immediate response to the presence of a pyrogen and the neural and humoral pathways activated that ultimately communicate these signals to the brain. In the course of these studies, we have uncovered several fever-triggering processes and delineated the trajectories of their pathways from the periphery to the brain. We have also described the neurochemical processes in the brain for febrigenesis, and developed a conceptual model of the afferent and central mechanisms involved. These are depicted in the diagram to the right.
From a total of 133:
- Li, S., J. Llanos-Q, and C.M. Blatteis. Thermal Response to Zymosan: The Differential Role of Complement. Neuroimmunomodulation. 10:122-128, 2003.
- Feleder, C., Z. Li, V. Perlik, A. Evans, and C.M. Blatteis. The Spleen Modulates the Febrile Response of Guinea Pigs to LPS. Am. J. Physiol. Regu. Integr. Comp. Physiol. 284: R1466-R1476, 2003.
- S. Li, S. Goorha, L.R. Ballou, and C.M. Blatteis. Intracerebroventricular Interleukin-6, Macrophage Inflammatory Protein-1b, and IL-18: Pyrogenic and PGE2-Mediated? Brain Res. 992:76-84, 2003.
- Li, Z., and C.M. Blatteis. Fever Onset Is Linked to the Appearance of Lipopolysaccharide in the Liver. J. Endotoxin Res. 10:39-53, 2004.
- Feleder, C., V. Perlik, and C.M. Blatteis. Preoptic a1 and a2 Noradrenergic Agonists Induce, Respectively, PGE2-Independent and PGE2-Dependent Hyperthermic Responses in Guinea Pigs. Am. J. Physiol. Regul. Integr. Comp. Physiol. 286:R1156-R1166, 2004.
- Li, Z., C. Feleder, and C.M. Blatteis. Lipopolysaccharide (LPS) Challenge Causes Exaggerated Fever and Increased Hepatic LPS Uptake in Vinblastine-Induced Neutropenic Guinea Pigs. Crit. Care Med. 32:2131-2134, 2004.
- Perlik V, Z. Li, S. Goorha, L.R. Ballou, and C.M. Blatteis. LPS-Activated Complement, not LPS per se, Triggers the Early Release of PGE2 by Kupffer Cells. Am. J. Physiol. Regul. Integr. Comp. Physiol. 289:R332-R339, 2005.
- Li S, S.A. Boackle, V.M. Holers, J.D. Lambris, and C.M. Blatteis. Complement Component C5a Is Integral to the Febrile Response of Mice to Lipopolysaccharide. NeuroImmunoModulation 12:67-80, 2005.
- Feleder, C., V. Perlik, Y. Tang, and C.M. Blatteis. Putative Antihyperpyretic Factor Induced by LPS in the Spleen of Guinea Pigs. Am. J. Physiol. Regul. Integr. Comp. Physiol. 289:R680-R687, 2005.
- Li, Z., V. Perlik, C. Feleder, Y. Tang, and C.M. Blatteis. Kupffer Cell-Generated PGE2 Triggers the Febrile Response of Guinea Pigs to Intravenously Injected LPS. Am. J. Physiol. Regul. Integr. Comp. Physiol. 290:R1262-R1270, 2006.
- Feleder, C., V. Perlik, and C.M. Blatteis. Preoptic Norepinephrine Mediates the Febrile Response of Guinea pigs to Lipopolysaccharide. Am. J. Physiol. Regul. Integr. Comp. Physiol. 293:R1135-R1143, 2007.
- Feleder, C., V. Perlik, and C. M. Blatteis. Preoptic Nitric Oxide Attenuates Endotoxic Fever in Guinea Pigs by Inhibiting the POA Release of Norepinephrine. Am. J. Physiol. Regul. Integr. Comp. Physiol. 293:R1144-R1151, 2007.
- Li, S., M.D. Breyer, C.B. Saper, and C.M. Blatteis. Prostaglandin E2 Receptors (EPR) 1 and 4 Do Not Mediate Lipopolysaccharide Fever in Mice. Am. J. Physiol. Regul. Integr. Comp. Physiol. (in preparation).
- Li, S., W. Dou, Y. Tang, S. Goorha, L.R. Ballou, and C.M. Blatteis. Acetaminophen: Antipyretic or Hypothermic in Mice? In Either Case, PGHS-1b (COX-3) iIs Irrelevant. Prostaglandins & other Lipid Mediat. 2007 Nov 12; [Epub ahead of print].
- Perlik, V., C. Feleder, L. L. Tague, and C. M. Blatteis. Febrile Responses of Unrestrained and Restrained Guinea Pigs to Lipopolysaccharide: Comparison of Two Thermometric Methods. Physiol. Behav. (in preparation).