Effect of hyperbaric oxygenation on macrophage function in mice

Inamoto, Yoshihito; Okuno, Fumio; Saito, Kazuyoshi; Tanaka, Yoshiya; Watanabe, Kenichi; Morimoto, Isao; Yamashita, Uki; Eto, Sumiya

doi:10.1016/0006-291x(91)91901-n

Cited by 50 publications

(31 citation statements)

References 9 publications

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“…One of the early studies showed that patients with rheumatoid arthritis who were treated with HBO achieved a remarkable recovery, suggesting that HBO has an immunosuppressive eect (Kamada 1985). This is supported by animal studies in which it was shown that HBO inhibits interleukin (IL)-1 production (Inamoto et al 1991;Saito et al 1991). One recent study has shown that HBO attenuates the production of TNF-a, IL-6, and their respective hepatic mRNAs after massive hemorrhage (Yamashita and Yamashita 2000).…”

Section: Discussionmentioning

confidence: 92%

“…In animal studies, it has been shown that HBO reduces post-ischemic edema (Nylander et al 1985), stimulates aerobic metabolism to preserve energy-rich compounds (Nylander et al 1987;Yamada et al 1994), reduces venular neutrophil adherence and inhibits progressive adjacent arteriolar vasoconstriction of ischemic muscle (Zamboni et al 1993b), accelerates the recovery of crush injured peripheral nerves (Bradshaw et al 1996), rescues ®bers from ischemic degeneration (Kihara et al 1995), and salvages testes from torsion (Kolski et al 1998). HBO reduces lung neutrophil sequestration in rats with intestinal ischemia-reperfusion injury (Tjarnstrom et al 1999), and suppress in¯ammatory processes (Inamoto et al 1991).…”

Section: Introductionmentioning

confidence: 96%

“…HBO enhances restoration of the circulation and function of injured limbs (Marucha et al 1991), it improves healing of skin grafts and¯aps (Zamboni et al 1993a), promotes functional recovery of injured peripheral nerves (Zao 1991) and limbs (Bouachour et al 1996), and ameliorates lymphadenopathy, hypergammaglobulinemia, butter¯y rash and protenuria of patients with systemic lupus erythematosus (Inamoto et al 1991). In animal studies, it has been shown that HBO reduces post-ischemic edema (Nylander et al 1985), stimulates aerobic metabolism to preserve energy-rich compounds (Nylander et al 1987;Yamada et al 1994), reduces venular neutrophil adherence and inhibits progressive adjacent arteriolar vasoconstriction of ischemic muscle (Zamboni et al 1993b), accelerates the recovery of crush injured peripheral nerves (Bradshaw et al 1996), rescues ®bers from ischemic degeneration (Kihara et al 1995), and salvages testes from torsion (Kolski et al 1998).…”

Section: Introductionmentioning

confidence: 98%

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Hyperbaric O 2 reduces intestinal ischemia-reperfusion-induced TNF-α production and lung neutrophil sequestration

Yang

Bosco

Montante

et al. 2001

European Journal of Applied Physiology

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Treatment with hyperbaric O2 (HBO) ameliorates ischemia-reperfusion (I/R) injury. Since tumor necrosis factor-alpha (TNF-alpha) plays an important role in I/R injury, we hypothesized that the effect of HBO in I/R injury may be due to its ability to inhibit TNF-alpha production. In this study, one group of rats received HBO during 60 min of ischemia (HBO group, n = 9), while control rats endured the same procedure but did not receive HBO (non-HBO, n = 9). A group of sham-operated control rats (SHAM, n = 6) underwent laparotomy without occlusion of the artery and HBO treatment. Intestinal I/R led to an increase in serum TNF-alpha concentration to [mean (SEM)] 165 (32) pg/ml (P < 0.01 vs SHAM rats). HBO attenuated this increase [34 (9) pg/ml; P<0.05 vs non-HBO group]. Intestinal I/R also resulted in a marked increase in lung myeloperoxidase content [0.62 (0.04) U/g vs 0.17 (0.02) U/g of SHAM rats, P<0.01]. HBO suppressed this increase [0.40 (0.04) U/g, P<0.05 vs non-HBO rats]. HBO ameliorated the injury to the intestine and lung. The number of neutrophils sequestered in the lung was reduced in HBO rats compared to non-HBO rats [6.4 (0.9) neutrophils/per oil field and 10.9 (2) neutrophils/per oil field, respectively; P < 0.05]. These findings demonstrate that HBO inhibits TNF-alpha production during intestinal I/R, and this reduced TNF-alpha production may be attributed to the beneficial effects of HBO.

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Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 98%

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Hyperbaric O 2 reduces intestinal ischemia-reperfusion-induced TNF-α production and lung neutrophil sequestration

Yang

Bosco

Montante

et al. 2001

European Journal of Applied Physiology

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“…Although beneficial, HBO may also be toxic and may affect immune responses, which are of the utmost importance in most of these conditions. Only limited information is currently available regarding the effect of a therapeutic hyperbaric oxygen profile on the immune system in normal and pathologic conditions [3][4][5]. In previous studies [6,7] we tested the effects of a single commonly used profile of exposure to hyperbaric oxygen on mononuclear cell subsets in healthy human volunteers and in an animal model.…”

Section: Introductionmentioning

confidence: 99%

Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-α) secretion from rat macrophages

Lahat

Bitterman

Yaniv

et al. 1995

Clinical and Experimental Immunology

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SUMMARYWe investigated the secretion of TNF-a by monocytes and macrophages derived from the peripheral blood, spleen, and lungs after a single exposure to a therapeutic profile of hyperbaric oxygen (HBO). Rats were exposed for 90 min to either 100% oxygen at 0 28 MPa (2-8 atmospheres absolute) or air. Immediately after exposure, mononuclear cells were isolated from blood, spleen, and lungs and cultured for 18h. The secretion of TNF-a from the cultured monocytes/macrophages was determined with and without stimulation with lipopolysaccharide (LPS). Exposure to hyperbaric oxygen induced a significant increase in the spontaneous ex vivo secretion of TNF-a (without LPS) by mononuclear cells from the blood, spleen, and lung (P < 0 05 from air controls). Stimulation with LPS after exposure to HBO induced a significant increase in TNF-a secretion by lung and spleen macrophages compared with air controls (P<005). However, absolute TNF-a levels were not significantly higher than those achieved 'spontaneously' in macrophages exposed to HBO without LPS. Stimulation with LPS induced a marked increase in secretion of TNF-a from blood monocytes after exposure to air, but not after exposure to HBO. These results provide evidence in support of a role played by TNF-a in mediating HBO effects on different tissues and their immune responses.

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“…In general, the effects of HBO are similar to those accomplished with immunosuppressant drugs, leading to a decrease in inflammatory response in the body [4,35], which is achieved by reducing the synthesis of inflammatory mediators such as nitric oxide (NO) [36,37], prostaglandin E2 (PGE2) [38,39], tumour necrosis factor α (TNF-α), interleukin 1β and 12 (IL-1β, IL-12) and interferon γ (IFN-γ) [9,16,18,23,38,40,41], as well as a reduced expression of cyclooxygenase-type 2 mRNA (COX-2), an enzyme involved in inflammation [42]. In addition to the inhibitory effect on the synthesis of proinflammatory cytokines, the consequence of hyperbaric oxygen therapy is an increased release of antiinflammatory cytokines such as interleukin 10 (IL-10) [9,43].…”

Section: Research Results and Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Therapy (HBOT) as a Therapeutic Option for Patients with Atopic Dermatitis (AD) – Own Experiences and Literature Review

Olszański¹,

Konarski

Siermontowski³

2017

Polish Hyperbaric Research

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The paper discusses the treatment results of ten patients with severe atopic dermatitis (AD) who did not respond to standard pharmacotherapy and underwent hyperbaric oxygen therapy (HBOT). Each patient was subject to 10 oxygen exposures at pO2 2.5 ATA (~ 250 kPa) with the duration time of 60 minutes. In the period of implementation of the hyperbaric procedures the general treatment plan was suspended for all patients while maintaining typical local treatment. Clinical evaluation was performed in the study group as well as determination of levels of immunoglobulins: IgA, IgG, IgM and IgE and C3 and C4 complement. All patients indicated clinical improvement and a decreased IgE immunoglobulin and complement C3 level upon the completion of the exposure cycle. Taking into account the authors' own observations and data from literature, an overall improvement in the clinical status and a decrease in the level of immunoglobulin E and C3 complement following a cycle of exposures may be indicative of an immunomodulating HBOT effect on AD, whereas hyperbaric oxygenation may constitute a therapeutic option for some patients with AD, especially those exhibiting a poor response to standard treatment.

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Effect of hyperbaric oxygenation on macrophage function in mice

Cited by 50 publications

References 9 publications

Hyperbaric O 2 reduces intestinal ischemia-reperfusion-induced TNF-α production and lung neutrophil sequestration

Hyperbaric O 2 reduces intestinal ischemia-reperfusion-induced TNF-α production and lung neutrophil sequestration

Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-α) secretion from rat macrophages

Hyperbaric Oxygen Therapy (HBOT) as a Therapeutic Option for Patients with Atopic Dermatitis (AD) – Own Experiences and Literature Review

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