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. 2017 Oct 23;18(10):2219. doi: 10.3390/ijms18102219

Table 3.

Studies demonstrating the pro-inflammatory capacity of LPS.

Authors Model Origin of LPS LPS Dose and Pathway Used Allergen or Antigen Allergen Dose and Pathway Used for Sensitization Allergen Dose and Pathway Used for Challenging Protocol Result Note
Rittirsch et al., 2008 [67]

  1. C57BL/6 mice

  2. C57BL/6 mice with neutrophil depleted by antibody

 Escherichia coli (serotype O111:B4) 50 μg LPS in 40 μL PBS intratracheally, total 2,550,100 μg nil nil nil Permeability index checked from bronchoalveolar lavage at 0, 2, 4, 6, 8 h.

  1. Maximal permeability at 50 μg, no different from 100 μg; at 6 h, no different from 8 h.

  2. When neutrophils depleted, no permeability change.

  3. Pathology includes: interstitial and intraalveolar deposits of neutrophils and fibrin, prominence of alveolar macrophages, and intraalveolar hemorrhage.

 The LPS concentration used is 1250 μg/mL, as compared to the 0.3 and 30 μg/mL in cell line model [9], and the total LPS used is 50 μg, as compared with total 100 ng to 1 μg LPS in Schuijs’ study [10].
Eutamene et al., 2005 [70]

  1. Male Wistar rats

  2. NCI-H292 human airway epithelial cells

  1. Pseudomonas aeruginosa

  2. Escherichia coli (SO55:B5)

  1. 1 μg LPS per rat via intra-tracheal instillate

  2. 2 μg/mL LPS for co-culture

 nil nil nil

  1. LPS from P. aeruginosa instilled in the trachea at a constant rate of 10 μL/min for 15 min.

  2. LPS from E. coli for 15 and 30 min and 1, 2, 3 and 6 h.

  1. Airway epithelial paracellular permeability was increased , Leukocytes number in BAL fluid was sixfold higher, with macrophage, neutrophil and lymphocyte numbers significantly increased.

  2. Myosin light chain (MLC) phosphorylation occurs after E. coli co-culture, and tight junction permeability increased.

 P. aeruginosa is a strong pathogen for airway [71], so total amount of LPS used is less, as compared with studies above.
Rojas et al., 2005 [68] C57BL/6 male mice Escherichia coli O111:B6 Intraperitoneally with 1 mg/kg LPS nil nil nil Mice were inoculated intraperitoneally with 1 mg/kg of LPS from E. coli O111:B6. Sublethal dose of i.p. LPS to mice caused rapid onset of interstitial pulmonary edema, inflammatory cell accumulation, and deposition of fibronectin and collagen in the lungs. The scale of mg/kg is sublethal, compared to the protective dose scale of ng/mL to μg/mL.
Yao et al., 2017 [69]

  1. Male C57BL/6J mice

  2. male Wistar rats

 LPS, source not specified

  1. i.p. LPS at the doses of 8 mg/kg

  2. i.p. LPS at the doses of 5 mg/kg

 nil nil nil Lung injury in mice and rats were induced by i.p. LPS. Lung tissues revealed interstitial edema and hemorrhage, alveolar wall thickening, increased infiltration of neutrophils and macrophages in the lung parenchyma and alveolar spaces. Again, the dose of causing acute lung injury is on the scale of mg/kg.
Taveira da Silva et al., 1993 [72] Human Salmonella minnesota i.v. LPS nil nil nil The patient administered i.v. 1 mg of S. minnesota LPS, in sterile water, in an attempt to treat a tumor. Septic shock syndrome induced, including a high-cardiac-output hypotension, disseminated intravascular coagulation, abnormalities of hepatic and renal function, and non-cardiogenic pulmonary edema. 1 mg of purified LPS is equivalent to 15,000 ng/kg, thousands times higher than the usual dose of 4 ng/kg given to normal volunteers in experimental studies. Endothelial cells are much more sensitive to LPS than epithelial cells, with pg/mL level LPS activating endothelial cells in the presence of blood, compared to the relative resistance of respiratory epithelial cells to μg/mL level LPS [66].
Pugin et al., 1993 [66] Human umbilical vein endothelial cells (HUVEC)

  1. Escherichia coli 0111:B4

  2. Salmonella minnesota

 Incubated with different dilutions of E. coli 0111:B4 or S. minnesota wild-type LPS, from 10−1 to 104 pg/mL nil nil nil HUVECs incubated with different dilutions of LPS for 6 h In the presence of whole blood, 1000-fold less LPS was required to achieve the level of HUVEC activation (assessed by VCAM-1 upregulation) observed with plasma alone. Endothelial cells are sensitive to ng/mL LPS in the absence of blood, but much more sensitive even to pg/mL LPS in the presence of blood.
Rodriguez et al., 2003 [54] C57BL/6J, BALB/c and C3H/HeJ mice Salmonella abortus equi LPS at a dose of 20 μg/animal was delivered intranasally concomitantly with a second OVA challenge OVA 4 μg OVA/1.6 mg aluminum hydroxide 10 μg OVA/50 μL saline intranasally Mice were immunized on Days 0 and 7, and challenged on Days14 and 21 intranasally

  1. LPS administration suppresses allergic airway inflammation and cytokine production through a mechanism independent of IL12 or IFNγ

  2. Local LPS switched the airway inflammation from eosinophilia to neutrophilia.

  3. Local LPS increased AHR by neutrophilic inflammation.

 Systemic LPS displayed protective effect, while local LPS displayed pro-inflammatory effect with neutrophilia reaction.
Hammad et al., 2009 [62] Radiation-induced chimeric Tlr4-deficient mice with DCs deficient or ECs-like cells Rhodobacter sphaeroides 10 μg or 100 ng per mouse, in 80 μL PBS, intratracheal HDM nil Intratracheal 100 μg HDM 80 μL PBS intratracheal with HDM and LPS TLR4 expression on lung structural cells, but not on DCs, is necessary and sufficient for lung DC activation and for priming of effector T helper responses to HDM. TLR4 triggering on structural cells in the presence of HDM caused production of TSLP, GM-CSF, IL25 and IL33. The absence of TLR4 on structural cells, but not on hematopoietic cells, abolished HDM-driven allergic airway inflammation.

nil: not in list.