Effect of Influenza Virus Infection on Phagocytic and Cytopeptic Capacities of Guinea Pig Macrophages

Taylor, Roger N.; Dietz, Thomas; Maxwell, Kameron W.; Marcus, Stanley

doi:10.3109/08820137409061124

Cited by 14 publications

(8 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since areas of consolidation could not be easily discerned on sections of virus-infected lungs stained (10), and alveolar macrophages (11). A prominent shortcoming of these studies, however, was that they were performed in vitro.…”

Section: Methodsmentioning

confidence: 99%

Defect in intracellular killing of Staphylococcus aureus within alveolar macrophages in Sendai virus-infected murine lungs.

Jakab¹,

Green²

1976

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Bacterial multiplication associated with virus infections is related to defects in in situ bactericidal (phagocytic) mechanisms of the lung. To determine whether the phagocytic defect was in bacterial ingestion and/or intracellular digestion, mice were infected with a sublethal dose of aerosolized Sendai virus and challenged 7 days later with a finely dispersed aerosol of Staphylococcuts aureus. Groups of uninfected and virus-infected mice were sacrificed at 0, 6, 12, and 24 h after challenge, the lungs were perfused with formalin in situ, and the intra-or extracellular location of the bacteria was determined histologically. At 0 h, 49% and 51% of the staphylococci had an intracellular location in virus and nonvirus-infected lungs, respectively. With time, decreasing numbers of staphylococci were observed within the phagocytic cells of nonvirus-infected lungs, mostly as single organisms or in small clusters of less than four. Ill contrast, in focal area of virus-infected lungs, increasing numbers of phagocytic cells showed clumps of more than 25 bacteria/cell. These data demonstrate that virus-infected suppression of pulmonary antibacterial activity against S. aureus is related primarily to defects in intracellular processing mechanisms.

show abstract

Section: Methodsmentioning

confidence: 99%

Defect in intracellular killing of Staphylococcus aureus within alveolar macrophages in Sendai virus-infected murine lungs.

Jakab¹,

Green²

1976

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…In this respect, we observed that although swine influenza virus does not replicate completely in SAM, another virus, namely the porcine coronavirus TGEV (transmissible gastroenteritis virus), does multiply in SAM, inducing cell lysis and interferon production (Laude and Charley, in press). Virus-macrophage interactions can be modified by immune responses [27,16,18]: in the case of vaccinia virus, for example, virus uptake by macrophages is enhanced by antibodies, and the neutralized virions are sequestered within lysosomes, where they are degraded [22]. From the present data, it appears that antibodies suppress the SAM lysis by influenza virus: this could mean either that antibodies neutralize extracellular virus particles, or that they opsonize the virus and stimulate its phagocytosis.…”

Section: Discussionmentioning

confidence: 81%

“…Alveolar macrophages are important elements in the lungs' defence mechanisms against infection, being capable of phagocytosis [30], cellmediated cytotoxicity [25], interferon production [1] and numerous interactions with the immune system [12]. In the course of an influenza infec-tion, secondary bacterial pneumonias are often described and are partly explained by impaired functions of the alveolar macrophages; thus, influenzavirus-infected mice showed a reduced rate of inactivation of inhaled bacteria I331 as well as altered alveolar maerophage activities [27,13]. Quite similar results were obtained with Sendai (parainfluenza 1) virus infection in mice [8,23,32].…”

Section: Introductionmentioning

confidence: 99%

Interaction of influenza virus with swine alveolar macrophages: Influence of anti-virus antibodies and cytochalasin B

Charley¹

1983

Annales de l'Institut Pasteur / Virologie

View full text Add to dashboard Cite

“…A variety of virus infections are associated with a dysfunction of the phagocytic cells. Influenza viruses have been most widely studied in this respect and were demonstrated to diminish phagocytosis, intracellular killing, and chemotaxis in humans (17,19), guinea pigs (29), chinchillas (1), rats (25), and mice (15). Impaired phagocytic cell function was observed with other viruses including Sendai virus (13), respiratory syncytial virus (8), infectious bovine rhinotracheitis virus (11), mumps virus (22), herpes simplex virus (24), and cytomegalovirus (26).…”

mentioning

confidence: 99%

Depressed chemiluminescence response by influenza virus is enhanced after conjugation of viral subunits to muramyl dipeptide

Kn¹,

Lange²,

Rohde-Schulz³

et al. 1985

Infect Immun

View full text Add to dashboard Cite

The effect on respiratory burst of murine spleen cells after in vitro exposure to influenza virus, subunits, or subunits conjugated to muramyl dipeptide (MDP) was studied by luminol-dependent chemiluminescence (CL) in response to stimulation by zymosan. CL induced by infectious influenza A virus was depressed but could be elevated to normal levels when MDP was added together with a low, but not with a high, dose of the virus. Profound depression of CL was induced by high doses of influenza A/Brazil, A/Bangkok, and B/Singapore subunits. The same amounts of viral subunits conjugated to MDP restored or even enhanced the CL responses of spleen cells from BALB/c and C57BL/6 mice. Splenic cells from BALB/c mice generated higher levels of CL than did cells from C57BL/6 mice.

show abstract

Effect of Influenza Virus Infection on Phagocytic and Cytopeptic Capacities of Guinea Pig Macrophages

Cited by 14 publications

References 13 publications

Defect in intracellular killing of Staphylococcus aureus within alveolar macrophages in Sendai virus-infected murine lungs.

Defect in intracellular killing of Staphylococcus aureus within alveolar macrophages in Sendai virus-infected murine lungs.

Interaction of influenza virus with swine alveolar macrophages: Influence of anti-virus antibodies and cytochalasin B

Depressed chemiluminescence response by influenza virus is enhanced after conjugation of viral subunits to muramyl dipeptide

Contact Info

Product

Resources

About