Temperature Effects on <i>Legionella pneumophila</i> Killing by and Multiplication in Phagocytes of Guinea Pigs

Miyamoto, Hiroshi; Ogawa, Midori; Maruta, Koji; Nikaido, Yoshihiko; Yamamoto, C.; Taniguchi, Hatsumi; Yoshida, Shigeaki

doi:10.1111/j.1348-0421.1995.tb03252.x

Cited by 12 publications

(11 citation statements)

References 32 publications

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“…1 as the 10glO increase in the number of CFU per well at intervals. An initial decrease in CFU was observed in NJ and C57BL/6 macrophages at 2 and 4 hr after in vitro phagocytosis, as previously reported on macrophages of guinea pigs (10). In CGD macrophages, however, hardly any initial killing was observed (Fig.…”

supporting

confidence: 66%

“…Colonies on the agar plates were counted four days after inoculation. ing 2-6 hr after phagocytosis in the same way as macrophages of guinea pigs (10). It was considered that this trait had no relation to the permissive nature of Legionella growth because initial decreases of CFU were equally observed in the macrophages of both NJ (susceptible) and C57BU6 (resistant) mice.…”

mentioning

confidence: 99%

“…Each well was washed twice with sterile cold PBS to remove nonphagocytosed bacteria, and then the cells were incubated in RPMI Medium 1640 containing 10% newborn calf serum at 37 C in a CO2 incubator. In this system, antibiotics which might influence intracellular bacterial growth were not used because L. pneumophila cannot grow extracellularly in RPMI Medium 1640 (10).…”

mentioning

confidence: 99%

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Fate of Legionella pneumophila in Macrophages of C57BL/6 Chronic Granulomatous Disease Mice

Saito

Kajiwara

Miyamoto

et al. 2001

Microbiology and Immunology

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Abstract:We compared the intracellular survival and growth of Legionella pneumophila Philadelphia-l in peritoneal macrophages obtained from AlJ, C57BLl6, and X-linked chronic granulomatous disease (CGO) mice produced from C57BLl6 strain. The initial killing was observed in AlJ and C57BLl6 macrophages at 2,4 and 6 hr after in vitro phagocytosis, but not in the CGO macrophages. Thereafter, there was a lO-fold increase of CFU in AlJ macrophages. The bacteria, however, did not proliferate in C57BLl6 and CGO macrophages at 24 or 48 hr after in vitro phagocytosis. These results suggest that effector molecules for the initial killing are a superoxide anion and its metabolites, and Lgnl gene product inhibits the intracellular growth of L pneumophila independently of NAOPH oxidase.

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confidence: 66%

mentioning

confidence: 99%

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confidence: 99%

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Fate of Legionella pneumophila in Macrophages of C57BL/6 Chronic Granulomatous Disease Mice

Saito

Kajiwara

Miyamoto

et al. 2001

Microbiology and Immunology

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“…In addition to A. phagocytophilum, several other pathogens such as Legionella pneumophila (Miyamoto et al 1995), the bovine pathogenic bacterium Haemophilus somnus (Czuprynski and Hamilton 1985), the fungal pathogen Histoplasma capsulatum (Medeiros et al 2002), and Burkholderia pseudomallei (Egan and Gordon 1996), the causative agent of melioidosis, were observed to multiply in PMN. Earlier studies demonstrated the intracellular survival of Chlamydia psittaci and Chlamydia trachomatis in PMN (Register et al 1986).…”

Section: Survival Of Pathogens Inside Neutrophilsmentioning

confidence: 98%

Neutrophil granulocytes as host cells and transport vehicles for intracellular pathogens: Apoptosis as infection-promoting factor

2008

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“…The febrile rise in body temperature could exert beneficial effects for the host by enhancing immune cell activities (138) and making the internal thermal environment out of the temperature range optimal for pathogen growth (90). Increase in body temperature similar to fever is also observed when animals receive psychological stress.…”

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confidence: 95%

Central circuitries for body temperature regulation and fever

Nakamura

2011

American Journal of Physiology-Regulatory, Integrative and Comp

442

394

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Nakamura K. Central circuitries for body temperature regulation and fever. Am J Physiol Regul Integr Comp Physiol 301: R1207-R1228, 2011. First published September 7, 2011 doi:10.1152/ajpregu.00109.2011.-Body temperature regulation is a fundamental homeostatic function that is governed by the central nervous system in homeothermic animals, including humans. The central thermoregulatory system also functions for host defense from invading pathogens by elevating body core temperature, a response known as fever. Thermoregulation and fever involve a variety of involuntary effector responses, and this review summarizes the current understandings of the central circuitry mechanisms that underlie nonshivering thermogenesis in brown adipose tissue, shivering thermogenesis in skeletal muscles, thermoregulatory cardiac regulation, heat-loss regulation through cutaneous vasomotion, and ACTH release. To defend thermal homeostasis from environmental thermal challenges, feedforward thermosensory information on environmental temperature sensed by skin thermoreceptors ascends through the spinal cord and lateral parabrachial nucleus to the preoptic area (POA). The POA also receives feedback signals from local thermosensitive neurons, as well as pyrogenic signals of prostaglandin E 2 produced in response to infection. These afferent signals are integrated and affect the activity of GABAergic inhibitory projection neurons descending from the POA to the dorsomedial hypothalamus (DMH) or to the rostral medullary raphe region (rMR). Attenuation of the descending inhibition by cooling or pyrogenic signals leads to disinhibition of thermogenic neurons in the DMH and sympathetic and somatic premotor neurons in the rMR, which then drive spinal motor output mechanisms to elicit thermogenesis, tachycardia, and cutaneous vasoconstriction. Warming signals enhance the descending inhibition from the POA to inhibit the motor outputs, resulting in cutaneous vasodilation and inhibited thermogenesis. This central thermoregulatory mechanism also functions for metabolic regulation and stress-induced hyperthermia.

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Temperature Effects on Legionella pneumophila Killing by and Multiplication in Phagocytes of Guinea Pigs

Abstract: Abstract:We examined the effects of temperature

Cited by 12 publications

References 32 publications

Fate of Legionella pneumophila in Macrophages of C57BL/6 Chronic Granulomatous Disease Mice

Fate of Legionella pneumophila in Macrophages of C57BL/6 Chronic Granulomatous Disease Mice

Neutrophil granulocytes as host cells and transport vehicles for intracellular pathogens: Apoptosis as infection-promoting factor

Central circuitries for body temperature regulation and fever

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