Macrophages and Other Nonspecific Defenses: Role in Modulating Resistance Against Herpes Simplex Virus

Wu, Linxian; Morahan, Page S.

doi:10.1007/978-3-642-77247-4_6

Cited by 28 publications

(21 citation statements)

References 77 publications

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“…In the lungs, infectious virus was not detected up to five days after infection in control BALB/c and C57BL/6 mice, showing that macrophages in the spleen and liver usually filtrate MCMV particles and protect other organs from rapid dissemination of MCMV after intravenous infection. Generally, two types of macrophage-mediated resistance mechanisms against HSV have been demonstrated (42). One mechanism is the ability of macrophages to inhibit virus replication in surrounding cells permissive for virus infection or to destroy infected cells which can be defined as extrinsic resistance.…”

Section: Discussionmentioning

confidence: 99%

“…One mechanism is the ability of macrophages to inhibit virus replication in surrounding cells permissive for virus infection or to destroy infected cells which can be defined as extrinsic resistance. The other one is the ability of macrophages to phagocytose and digest virus particles or to inhibit virus growth inside the macrophages themselves, defined as intrinsic resistance (42). First, the antiviral activity of macrophages against other permissive cells (21,22,36) was demonstrated in vitro.…”

Section: Discussionmentioning

confidence: 99%

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Role of Macrophages in Acute Murine Cytomegalovirus Infection

Hamano

Yoshida

Takimoto

et al. 1998

Microbiology and Immunology

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It has been recognized that macrophages play an important role in controlling virus infection in experimental animal models. To evaluate the role of macrophages in acute murine cytomegalovirus infection, macrophages in the spleen and the liver were eliminated by an intravenous injection of liposomes containing a cytolytic agent, dichloromethylene diphosphonate. The depletion of macrophages led to a significant increase of virus titer in the spleen and lungs in both susceptible BALB/c and resistant C57BL/6 mice during the first three days after intravenous infection. In the spleen, the increase of virus titer in macrophagedepleted BALB/c mice was much greater than that in NK cell-depleted mice. These results suggest that macrophages contribute to protection mainly by the mechanisms which are independent of NK cells during the first three days after infection. The increase of virus titer in macrophage-depleted C57BL/6 mice was as great as that in NK cell-depleted mice because of the high contribution of NK cells to protection in C57BL/6 mice. In the liver in both strains of mice, the effects of macrophage depletion on virus titer were not as much as those in the spleen and lungs. Furthermore, the local depletion of peritoneal macrophages resulted in a great increase of virus titer in the spleen at three days after intraperitoneal infection. We conclude that macrophages greatly contribute to decreasing the virus load in some organs possibly through either or both intrinsic and extrinsic mechanisms in the early phase of primary infection with murine cytomegalovirus.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Hamano

Yoshida

Takimoto

et al. 1998

Microbiology and Immunology

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“…Macrophages act as a first line of defense in eliminating viral pathogens by inhibiting virus growth within itself, as well as to inactivate extracellular virus, suppress virus replication in adjacent cells, and destroy infected cells (46). Alveolar and peritoneal macrophage antiviral resistance to HSV is reduced in mice following exercise to fatigue (10,12), as is macrophage antigen presentation (7).…”

mentioning

confidence: 99%

Benefits of oat β-glucan on respiratory infection following exercise stress: role of lung macrophages

Murphy

Davis²,

Brown³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Exercise stress is associated with an increased risk for upper respiratory tract infection (URTI). We have shown that consumption of the soluble oat fiber β-glucan (OβG) can offset the increased risk for infection and decreased macrophage antiviral resistance following stressful exercise; however, the direct role of macrophages is unknown. This study examined the effect of macrophage depletion on the benefits of orally administered OβG on susceptibility to infection (morbidity, symptom severity, and mortality) following exercise stress. CL2MDP (Ex- H2O-CL2MDP, Ex-OβG-CL2MDP, Con-H2O-CL2MDP, Con-OβG-CL2MDP)-encapsulated liposomes were administered intranasally to deplete macrophages, and PBS (Ex-H2O-PBS, Ex-OβG-PBS, Con-H2O-PBS, Con-OβG-PBS)-encapsulated liposomes were given to macrophage-intact groups. Ex mice ran to volitional fatigue on a treadmill for 3 consecutive days, and OβG mice were fed a solution of 50% OβG in their drinking water for 10 consecutive days before infection. Fifteen minutes following the final bout of Ex or rest, mice were intranasally inoculated with 50 μl of a standardized dose of herpes simplex virus-1. Ex increased morbidity ( P < 0.001) and symptom severity ( P < 0.05) but not mortality ( P = 0.09). The increase in morbidity and symptom severity was blocked by OβG consumption for 10 consecutive days before exercise and infection [morbidity ( P < 0.001) and symptom severity ( P < 0.05)]. Depletion of macrophages negated the beneficial effects of OβG on reducing susceptibility to infection following exercise stress, as evidenced by an increase in morbidity ( P < 0.01) and symptom severity ( P < 0.05). Results indicate that lung macrophages are at least partially responsible for mediating the beneficial effects of OβG on susceptibility to respiratory infection following exercise stress.

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“…Viral replication was examined in the lungs of B6, B6.IL-12 Ϫ/Ϫ , and B6.IL-18 Ϫ/Ϫ mice at various times after intranasal infection with 10 6 PFU of HSV-1 (Fig. 2B).…”

Section: Exacerbation Of Disease In B6il-18 ϫ/ϫ Mice Following Intramentioning

confidence: 99%

“…To determine the effects of IL-12 or IL-18 deficiency on lung inflammation, we characterized the immune cells recovered in the BALF from B6, B6.IL-12 Ϫ/Ϫ , and B6.IL-18 Ϫ/Ϫ mice after intranasal infection with 10 6 PFU of HSV-1. BALF cell numbers increased transiently following infection, peaking at day 7 and declining thereafter (Fig.…”

Section: Inflammatory Cell Counts In Balf Are Increased In B6il-18 ϫmentioning

confidence: 99%

IL-18, but not IL-12, Regulates NK Cell Activity following Intranasal Herpes Simplex Virus Type 1 Infection

Reading

Whitney

Barr

et al. 2007

The Journal of Immunology

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Infection of the respiratory tract with HSV type 1 (HSV-1) can have severe clinical complications, yet little is known of the immune mechanisms that control the replication and spread of HSV-1 in this site. The present study investigated the protective role of IL-12 and IL-18 in host defense against intranasal HSV-1 infection. Both IL-12 and IL-18 were detected in lung fluids following intranasal infection of C57BL/6 (B6) mice. IL-18-deficient (B6.IL-18−/−) mice were more susceptible to HSV-1 infection than wild-type B6 mice as evidenced by exacerbated weight loss and enhanced virus growth in the lung. IL-12-deficient (B6.IL-12−/−) mice behaved similarly to B6 controls. Enhanced susceptibility of B6.IL-18−/− mice to HSV-1 infection correlated with a profound impairment in the ability of NK cells recovered from the lungs to produce IFN-γ or to mediate cytotoxic activity ex vivo. The weak cytotoxic capacity of NK cells from the lungs of B6.IL-18−/− mice correlated with reduced expression of the cytolytic effector molecule granzyme B. Moreover, depletion of NK cells from B6 or B6.IL-12−/− mice led to enhanced viral growth in lungs by day 3 postinfection; however, this treatment had no effect on viral titers in lungs of B6.IL-18−/− mice. Together these studies demonstrate that IL-18, but not IL-12, plays a key role in the rapid activation of NK cells and therefore in control of early HSV-1 replication in the lung.

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Macrophages and Other Nonspecific Defenses: Role in Modulating Resistance Against Herpes Simplex Virus

Cited by 28 publications

References 77 publications

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Benefits of oat β-glucan on respiratory infection following exercise stress: role of lung macrophages

IL-18, but not IL-12, Regulates NK Cell Activity following Intranasal Herpes Simplex Virus Type 1 Infection

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